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bio > exam 2 BSC 2010 spielbauer > Flashcards

exam 2 BSC 2010 spielbauer Flashcards

1
Q

inheritance

A

traits passed from parents to offspring

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2
Q

blending inheritance

A

theory that genes of a child are a mix of the the parents

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3
Q

particulate inheritance

A

there are specific genes (parts) that are passed down from each parent, not just a mix of them

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4
Q

gregor mendel

A

father of genetics, did pea plant experiements, discovered particulate inheritance

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5
Q

cross-fertilization

A

fertilizing one plant with another plant

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6
Q

self-fertilization

A

fertalizing a plant with itself

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7
Q

character

A

observable physical features

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8
Q

trait

A

forms of characters (wrinkled vs smooth seeds)

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9
Q

true-breeding variety

A

always same color flower when crossed, same traits as parents

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10
Q

reciprocal cross

A

each plant recieves and donates pollen between each other

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11
Q

monohybrid cross

A

true breeding purple x true breeding white -> f1 -> selfed -> f2

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12
Q

P Generation

A

The parent generation, the originals

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13
Q

F1 generation

A

the first filial (child) generation

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14
Q

F2 Generation

A

the children of the F1, second filial generation

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15
Q

Gene

A

discrete particulate factors

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16
Q

Locus

A

place where DNA is

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17
Q

Allele

A

diff versions of the same gene

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18
Q

Genotype

A

what their genes are, ex AA or aa

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19
Q

Phenotype

A

How that gene is expressed, ex wrinkled or smooth

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20
Q

Dominant vs Recessive Allelle

A

Dominant is expressed over recessive

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21
Q

Law of Segreation

A

Allelles are segregated equally in gametes

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22
Q

Genotypic ratio

A

how their alleles were in relation (1:2:1)

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23
Q

Phenotypic ratio

A

how their appearance was in relation (3:1)

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24
Q

Test Cross

A

plant dominant phenotype (A-) is crossed with homo recessive (aa)

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25
Q
  1. Explain the differences between blending inheritance and particulate inheritance. What evidence did Mendel’s monohybrid cross uncover that supported particulate inheritance and didn’t make sense with blending inheritance?
A

blending inheritance suggests that the genes mix together - in the monohybrid cross, it wouldn’t make sense that there are 3 purple flowers and one white, they would all be light purple. In the next generation, it wouldn’t make sense that that 2 purple flowers would result in a white flower.

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26
Q
  1. Describe the two ways that Mendel controlled the mating of pea plants (involved pollen transfer) so he could know which parents produced specific offspring.
A

cross fertilization, chose the specific plants that he would transfer pollen to, and then also did a self hybrid in which he put the pollen on the same plant.

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27
Q
  1. What was the goal of Mendel’s experiments? What was he trying to understand?
A

How genes were passed on, and explain phenonmenon that did not makes sense with the idea of blending inheritance

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28
Q
  1. Explain the process that Mendel went through to do his monohybrid cross. Explain how he created the Parental generation, and F1 generation, and the F2 generation. What were the phenotypic ratios of each generation?
A

parental gen was created by true breeding crosses, f1 resulted in monohybrids(all Aa), and then f2 resultd in the 3:1 phenotypic ration and 1:2:1 genotypic ratio

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29
Q
  1. What patterns did Mendel observe in all 7 of his monohybrid crosses? How did the phenotypes present change from generation to generation? What about the phenotypic ratio in the F2 generation?
A

3:1 phenotypic ratio in the f2 generation

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30
Q
  1. Explain what is meant by the underlying 1:2:1 “potential offspring” ratio that Mendel saw in the F2 generation of his pea plant crosses. How did he find this underlying ratio? Why could some of the purple flowers produce white offspring, while the other purple flowers could not?
A

Some could produce white offspring because they both had the recessive allelle, and they could create a flower that had both recessive allelles so they became white, found the potential ration in the f3 generation

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31
Q
  1. Be able to define and explain the relationship between the terms: genes, alleles, genotype, phenotype, dominant, recessive, homozygous, and heterozygous.
A

genes are made up of allelles. the genotype is the allelles that an organism has and the phenotype is how they are expressed. Dominant genes express over recessive genes, and a homozygous organism has 2 of the same allelle and a heterozygous organism has 2 different allelles.

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32
Q
  1. Explain the Law of Segregation. What does it mean? And how does it relate to Mendel’s experiments?
A

each gamete recieves only one copy of an allelle

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33
Q
  1. Following the Law of Segregation, what alleles will an individual with Aa genotype put into each gamete? What about AA genotype? Or aa?
A

Aa (A, a, A, a) AA (A,A,A,A) aa(a,a,a,a)

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34
Q
  1. What is a Punnett square? What does it allow us to visualize? What do you write on the sides of the square, and what do you write in the intersections in the middle?
A

helps to vizualize the genetic probability of offspring

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35
Q
  1. Describe how a test cross works. What do these allow you to do?
A

allows you to find the genotype of a unknown dominant plant - if thye have white offspring they are hetero

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36
Q
  1. Imagine you did a test cross between an individual with a dominant phenotype but unknown genotype (A_) and a homozygous recessive individual (aa). If you got a phenotypic ratio of 50% dominant and 50% recessive, what genotype must the dominant parent (A_) have? Making a Punnett square may help.
A

Aa, because there is no way for the recessive phenotype to appear with a AA for the parent.

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37
Q

multiplication rule

A

multiply independt events to find the prob that they will both happen

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38
Q

independent events

A

one does not influence the other, the probabilities are seperate

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39
Q

addition rule

A

add probs of mutally exclusive events to find the probability of either happening (or)

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40
Q

mutually exclusive events

A

dont have anything to do with the other

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41
Q

law of independent assortment

A

genes are seperate from each other and go into gametes seperately

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42
Q

dihybrid cross

A

pairs of traits to show tht they assort independently

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43
Q

pedigree

A

diagram that shows the inheritance pattern in a family

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44
Q

rare dominant allele

A

dominant, but rarely expressed (every affected individual has affected parent)

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45
Q

rare recessive allelle

A

heterosygotes can carry but many not be affected (2 heterosygotes can result in the affected offspring with a ratio of 3:1 affected)

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46
Q
  1. Explain why it is possible for a Rr x rr cross to produce offspring that are all rr.
A

because everything is just probability, each child has a 50% chance of being rr

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47
Q
  1. Why can we relate pennies to genotypes and flip outcomes to alleles? Think about the Law of Segregation.
A

This is because each allelle has an equal chance of being in the gamete, so it is all chance just like a coin flip

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48
Q
  1. Explain the basic rules of probability. What is the probability of a guaranteed event, an impossible event, or an event with multiple outcomes?
A

100%, 0%, < 100%

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49
Q
  1. What is the probability of you and another person independently flipping pennies and both landing on heads? What rule of probability are you applying here?
A

1/4, multiplication

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50
Q
  1. Explain the Law of Independent Assortment. What does it imply about the possible combinations of alleles when you are looking at the inheritance patterns of two genes? (If alleles of different genes can assort independently, will you always see the same combination of alleles? Or can there be any combination?
A

since they assort independently, and two genes can be in any combinations. They aren’t linked to each other. for example, green peas dont necearrisly have to be round or yellow peas don’t neceassrily have to be wrinkly, its all about the probabilyt of them happening together.

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51
Q
  1. Assume you found that the probability of producing yellow seeds in a monohybrid cross is 3/4, and the probability of producing wrinkled seeds from a different monohybrid cross is 1/4. If the alleles follow the Law of Independent Assortment, how would you calculate the probability of yellow and wrinkled seeds being produced in a dihybrid cross? (Remember the rules of probability)
A

3/4 x 1/4 = 3/16

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52
Q
  1. Describe how Mendel did his dihybrid cross. How did the process compare to his monohybrid cross?
A

he tracked two different traits instead of just one

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53
Q
  1. Assuming alleles follow the Law of Segregation and the Law of Independent Assortment, what possible alleles can be given by the genotype RRYY? What about rryy? Or RrYy?
A

RRYY(RY, RY, RY, RY) rryy (ry, ry, ry, ry) RrYy(RY, Ry, rY, ry)

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54
Q
  1. What is a pedigree? What do they show us, and how are they useful? How do they relate to Mendel’s laws of Segregation and Independent Assortment?
A

shows patterns of familial inhertiance, can show how traits are given and then expressed in each generation and how it is random

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55
Q
  1. Describe the patterns seen in the pedigree of a rare dominant allele.
A

every affect person has an affected parent

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56
Q
  1. Describe the patterns seen in the pedigree of a rare recessive allele.
A

often hidden until two heterosygous parents have a kid, and the kid displays the trait.

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57
Q

Chromosomal Theory of Inheritance

A

chromosomes follow mendels laws, and thats how/why they work

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58
Q

Sex-linkage

A

breaks law of segregation, genes may only be carreid on specific sex chromosomes

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59
Q

sex chromosomes

A

xx (female) xy(male)

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60
Q

gene-linkage

A

genes taht are close to each other on the same chromosomes are usually assorted into gametes together (breaks law of independent assortment)

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61
Q

sex-linked inheritance

A

traits associated with a particular sex

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61
Q

x-linked recessive

A

males are much more likely to have them, have affected maternal grandfathers and can only pass it to their daughters

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62
Q

thomas hunt morgan

A

demonstrated that traits could be carreid on sex chromosomes - mostly on eye color in fruit fliies

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63
Q

hemizygous

A

only one copy of some genes, males

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64
Q

wild type

A

the more common one in the wild

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65
Q

alfred sturtevant

A

morgan’s student, discovered crossing over

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66
Q

gene mapping

A

map the genes on the allelle using percentages, can predict whehter the genes are more likely to cross over or not

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67
Q

centrimorgans(cM)

A

measurement of gene mapping on an allelle

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68
Q
  1. How is the law of segregation seen in the segregation of alleles and homologous chromosomes into gametes?
A

each gamete gets one copu of each homologous chromosome

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69
Q
  1. How is the law of independent assortment seen in the segregation of alleles and homologous chromosomes into gametes?
A

chromosomes are assorted into gamete independently of one another

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70
Q
  1. How does sex-linkage break the law of segregation?
A

since genes are sometimes only carried on one chromosome, females can only give an x an and males can only give an y to a son

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71
Q
  1. How does gene-linkage break that law of independent assortment?
A

its not exactly completely random as genes taht are closer together on chromosome are usually assorted into gametes together

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72
Q
  1. What is sex-linkage, and what piece of evidence did it provide that helped support the chromosomal theory of inheritance?
A

when genes are on a sex chromosome, and it supported the idea that genes are on chromosmes

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73
Q
  1. What is gene-linkage, and what piece of evidence did it provide that helped support the chromosomal theory of inheritance?
A

when chromosomes cross over, they are likely to stay together if they are closer, meanign that the recombinant frequence is lower - doesnt always happen

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74
Q
  1. What is sex-linked inheritance? What are the common features of a rare recessive x-linked disorder? How does sex-linkage help explain these patterns?
A

affects son, affects his maternal grandfather, daughters are carriers

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75
Q
  1. Describe Thomas Hunt Morgan’s experiment that led to the discovery of sex-linkage.
A

flies, red eye father, white eye mother, white eye son, which shows how the mother can give x chromosome to the son, also how the father’s dominant red eyes did not give the son red eyes /

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76
Q
  1. Explain why males cannot give an X chromosome to their sons but can give one to their daughters.
A

because for the son they have to give a y chromosome

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77
Q
  1. Explain how gene mapping works. What can we infer about genes by comparing the percent of recombinant offspring in crosses like Morgan’s (AaBb x aabb)?
A

if the recombinant percentages are high, they are likley far way from each other on the chromosome, and if they are low, they are likely close together

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78
Q
  1. What does a smaller percentage of recombinant offspring imply about the relative location of two genes on a chromosome? (in an AaBb x aabb test cross)
A

they are probably close together

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79
Q
  1. What does a larger percentage of recombinant offspring imply about the relative location of two genes on a chromosome? (in an AaBb x aabb test cross)
A

farther away from each other

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80
Q
  1. What does having 50% recombinant offspring imply about the relative location of two genes? (in an AaBb x aabb test cross)
A

farthest apart from each other

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81
Q
  1. If you got a recombinant frequency of 15% between genes A and B, a recombinant frequency of 10% between A and C, and a recombinant frequency of 5% between genes B and C, which gene would be between the other two on the chromosome?
A

A C B

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82
Q

incomplete dominance

A

intermediate phenotype

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83
Q

codominance

A

2 allelles of a gene display both at the same time ( blood)

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84
Q

discrete traits

A

clear categories depending on the allelles (purple v white flowers)

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85
Q

quantitiative traits

A

vary within a range (height, weight, etc)

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86
Q

polygenic trait

A

character affected by multiple genes (wheat kernels have 3 diff geners taht contribute to color)

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87
Q

pleiotropy

A

one gene affects multiple characters (gene for a diseases affects other parts of the body

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88
Q

epistasis

A

one gene can influence anothers gene’s impact on a character

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89
Q

phenotypic plasticity

A

enviornment can influence a gene’s impact on a character

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90
Q

lethal allele

A

causes the death of an empbryo when homozygous

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91
Q

lateral gene transfer

A

transfer of genetic material between individuals

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92
Q

conjunction

A

transfer of DNA between prokaryotes

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93
Q

transformation

A

DNA from the enviornment into the prokaryote

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94
Q

transduction

A

tranfer from one p to another through a virus

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95
Q

plasmids

A

circular DNA molecule distinct from the chromosome in prokaryotic cells

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96
Q

sex pilus

A

initiates contact btw cels

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97
Q

conjugation tube

A

tube that allows info to pass from donor to recipient (not recprical)

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98
Q

antibiotics

A

kills bacteria

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99
Q

antibiotic resistance

A

bacteria that survives passes on its resistant genes so the bacteria contineus to survive

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100
Q

alexander fleming

A

discovered penicillin the first antibiotic

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101
Q
  1. Diploids can only carry two copies of a gene in their cells. How is it possible for a gene to have more than two alleles?
A

it has other alleles, each diploid jsut carries two

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102
Q
  1. Explain the difference between incomplete dominance and codominance. (This can be tricky. Remember that incomplete dominance is the dominant allele not being fully dominant over the recessive, compared to codominance is two dominant alleles not being able to block the phenotype of the other, so they are both present.) Refer to the examples from class to make sure you know the difference.
A

incomplete results in the blending of the two phenotypes (light purple eggplants), whereas codominance displays both phenotypes fully (blood)

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103
Q
  1. Compare/contrast discrete and quantitative traits.
A

discrete -> either or , purple or white quantitiative -> scale, height weight

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104
Q
  1. Compare/contrast a polygenic trait and pleiotropy.
A

polygenic -> multiple genes influence one character
pleiotropyy -> one gene affect multiple characters

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105
Q
  1. How can pleiotropy allow one gene to impact multiple characteristics?
A

cycstic fibrosis, causes a problem that shows up in multiple places in the body

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106
Q
  1. What is epistasis? Describe an example.
A

one gene influences the expresssion of the other -> labs, they have one gene that says whether they are black or brown and another that says whether the color is deposited or not (if not they are yellow)

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107
Q
  1. What is phenotypic plasticity? Describe an example.
A

organisms phenotypes are variable depending on the enviornemnt

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108
Q
  1. What are lethal alleles? Describe an example. How are lethal alleles able to be maintained in a population?
A

allelles that kill the animal as an embryo, maintained through heterosygous carries who dont express it but can pass it on

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109
Q
  1. Describe lateral gene transfer, and compare it to vertical gene transfer (from parents to offspring).
A

one prokaryote to the next, not through parents and offspring

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110
Q
  1. Name and describe the three ways that prokaryotes use lateral gene transfer.
A

conjunction - create a lol conjunction tube and send over DNA, transformation - incorporation of genetic materal from the enviornment, transduction, prokaryote to virus to another prokaryote

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111
Q
  1. Describe the steps involved in bacterial conjugation involving the transfer of plasmids.
A

plasmid transfered through conjugation tube as a single strand, and then the other strand is recreated in the donor and recipient

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112
Q
  1. Explain antibiotic resistance and how it can spread in a population of prokaryotes. Why is this a problem?
A

the living bacteria have the genes to resist the antibiotic and then they lateral gene transfer to the other ones the stay alive genes and then they grow back stronger

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113
Q

DNA binding dyes

A

developed in the early 1900s

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114
Q

flow cytometry

A

tracked the amoutn of DNA, - S, G2, and M had twice as much DNA compareds to G1

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115
Q

transformation experiment

A

found that bacteria could incorporate env DNA into their own

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116
Q

r strain

A

non-deadly strain, when present with heat killed s strain, can be deadly

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117
Q

s strain

A

deadly strain, when heat killed is non deadly

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118
Q

dna-degrading protein

A

when added, the mice did not die

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119
Q

hershey-chase experiment

A

bacteriophages (virus) inject either a protein or DNA into bacteria to replicate themselves- found they injected DNA

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120
Q

bacteriophages

A

virus taht injects DNA into bacteria to repliate the virus

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121
Q

32 p isotope

A

tags the DNA

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122
Q

35 S isotope

A

tags the protein

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123
Q

centrifuge

A

whirly thingy that seperates the viruses and the bacteria, bacterial cells on the bottom

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124
Q

pellet

A

the lower part - had viral DNA

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125
Q

supernatant

A

upper part, proteins and the virus

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126
Q

nitrogenous bases

A

purines ( adenine and guanine) pyramindes (thymine and cytosine (smaller)

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127
Q

adenine

A

purine, big, binds with T

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128
Q

guanine

A

purine big, bind with C

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129
Q

thymine

A

pyraminde (small), binds with A

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130
Q

cytosine

A

pyramidine (small), bind with G

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131
Q

purines

A

A+G

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132
Q

pyrimidines

A

T + C

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133
Q

erwin chargaff

A

discovered that there was an equal amount of purines to pyrimidines

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134
Q

rosalind franklin

A

created an image of the atoms in DNA

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135
Q

x-ray crystallography

A

xray source to a lead screan to aDNA sample that imprinted on a photographic plate

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136
Q

watson and crick

A

combined the knlowdge of DNA to determine the strucutre

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137
Q

antiparallel strands

A

found taht the strands must be the opposite of the other

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138
Q

complementary base pairing

A

A must go with T and C must go with G

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139
Q

semiconservatie replication hypothesis

A

each parental strand is a template for a new strand

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140
Q

conservative replication hypothesis

A

both strands act as a single tamplate and produce one fully daughter molecule

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141
Q

dispersiec replication hypothesis

A

parent is dispersed among 2 daughter molecules

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142
Q

meselson stahl experiment

A

found that DNA replication was semi conservative

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143
Q

15 n

A

dense DNA indicator

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144
Q

14 n

A

the medium, the default

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145
Q

DNA replication intiation

A

unwindig the double helix and synthesizing RNA primers

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146
Q

dna replication elongation

A

synthesizing new strands of DNA using each of the strands a a template

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147
Q

dna repliation termination

A

ends the synthesis of DNA

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148
Q

replication bubble

A

forms at the origin, creates a big bubble and lil forks pop up to start teh replication

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149
Q

replication fork

A

lil pieces that are ready to start the dna repliation, look more like combs tbh

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150
Q

DNA helicase

A

unzips ur genes

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151
Q

topoisomerase

A

untwists the DNA so it doesnt look like a twizzler

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152
Q

primase

A

creates short RNA strands that start the DNA

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153
Q

primers

A

lil RNA strands that start the DNA

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154
Q

dna polymerase

A

attaches to the primers and adds nucleotides to the 3’ end

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155
Q

5’ end

A

beginning

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156
Q

3’ end

A

end

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157
Q

leading strand

A

built continuously

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158
Q

lagging strand

A

built discontinuously

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159
Q

okazaki fragments

A

lil discontinous fragment

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160
Q

DNA ligase

A

joins the okazaki fragments together

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161
Q

end- replication problem

A

when the replication fork reaches the end of the chromosome, the leading strand is complete but the lagging strand has a lil piece cut off so the chromosome keeps getting shorter

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162
Q

telomeres

A

reptitice non-coding sequences at the ends of eukaryotic chromosomes to protect coding regions

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163
Q

telomerase

A

adds telomeres back on

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164
Q
  1. What was the circumstantial evidence that DNA is the molecule of inheritance? List and describe how each piece of evidence was discovered.
A

dna is present in the cell nucleus and in chromosomes, doubles during hte s phase of the cell cycle and there is twice as much in diploid cells vs haploid cells

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165
Q
  1. Describe the Transformation experiment, and how it provided strong evidence that DNA is the molecule of inheritance.
A

r strain and s strain, r strain is non deadly and the s train is deadly. when heat killed, the s strain is non deadly, but when added to the r strain it becomes deadly again. this is because there is DNA being communicated between the 2. Then when adding a dna degrading protein, it is non deadly again, meaning DNA is what is transferring genetic information

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166
Q
  1. Describe the Hershey-Chase experiment, and how it provided strong evidence that DNA is the molecule of inheritance.
A

bacteriophages are virsuses that inject something into bacteria to create more of themselves. In order to see what they injected, they radioactively tagged phosporous (to identify DNA) and sulfur (to identify proteins) and put them in a centrifuge. They knew the virus would be on the top and the bacteria would be on the bottom, so they wanted to see which tagged thing would be on teh top or bottom. dound phosphorous on the bottom, concluded they were injecting DNA

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167
Q
  1. List the chemical components that compose DNA. Compare/contrast purines and pyrimidines.
A

phosophate and deoxyribose backbone, nucleic acid bases, adenine and guanine are purines and cytosine and thymine are pyrimidines. purines are bigger

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168
Q
  1. Describe the discovery made by Erwin Chargaff regarding the ratios of the bases found in DNA. Think about why these ratios help in our understanding DNA structure and function.
A

the amount of A and G = the amount of C and T

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169
Q
  1. Describe the discovery made by Rosalind Franklin regarding the shape of DNA.
A

discoveredi t was a helical molecule

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170
Q
  1. Describe the discovery regarding the structure of DNA that Francis Crick and James Watson found that Rosalind Franklin also discovered.
A

found that it was a helix with antiparallell strands

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171
Q
  1. Given everything discovered regarding the makeup and shape of DNA, describe its structure. What aspect of its structure allows both strands to contain the same genetic information?
A

anti parallell strands with complementary base paring so taht it can contain information in both strands

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172
Q
  1. Describe the three DNA replication hypotheses.
A

semi conservative - each strand gets a complemantary strand to create 2 new strands
conservative - original dna creates an entirely new copy
dispersive - the new and old dna is dispersive and share parts

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173
Q
  1. Describe how the Meselson-Stahl experiment was performed and how it provided evidence for the semiconservative DNA replication hypothesis.
A

n15 isntead of n14, but put in a n14 medium, and then the dna replicated - > first time, created intermediate weight DNA and then the second time it was have heavy and half light

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174
Q
  1. List and briefly describe the three steps of DNA replication.
A

intiation - elongation - termination

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175
Q
  1. Describe the initiation of DNA replication. Explain the function of DNA helicase, topoisomerase, primase, and primers.
A

repliaction bubble forms, replication forks form, and helicase unzips the genes while topoisomersase makes sure they dont turn into a twizzler, primerase makes primers which are little RNA segments that start the DNA

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176
Q
  1. Describe the elongation of DNA during replication. Compare/contrast the elongation of the leading and lagging strands. Which one is composed of Okazaki fragments? What does that mean, and how are they combined into a single, continuous DNA strand? Explain this process and the components involved.
A

lagging is made up of okazaki fragments because its made up of lil pieces taht ligasse stitches together. leading strand is chillin and continues onward and completely finishes

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177
Q
  1. Describe the termination of DNA replication. Compare/contrast termination when replication forks meet, when the leading strand reaches the end of the chromosome, and when the lagging strand reaches the end. What problem occurs when the lagging strand reaches the end of the chromosome? Why is this an issue?
A

leading strand ends normally, whole thing is replicated, where as the lagging strand has a little bit cut offf, but its ok bc telomeres

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178
Q
  1. Describe the end-replication problem. How are we able to overcome this problem?
A

at the end of replication a bit of DNA is cut off

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179
Q
  1. Describe what a telomere is and how they work.
A

little bit at the end of the chromosome that doesnt mean anything

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180
Q
  1. Describe telomerase and how it functions.
A

creates new code for the telomere so taht they can keep getting cut off

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181
Q

somatic mutation

A

occur in somatic/body cells - can impact individual but do not impact offspring

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182
Q

germline mutation

A

occur in gametes and are passed to offspring and future generations

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183
Q

incorporation error rate

A

the probability that an incorrect base wll be inserted is about 1 in 100,000

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184
Q

nucleotide mismatch

A

when an incorrect base is input and it doesn’t match - quickly repaired

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185
Q

proofreading

A

when it recognizes a mismatch, backs up and then fixes itself

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186
Q

mismatch repair

A

protein complexes scan the DNA for wacky hydrogen bodning and removes/replaces the nucleotide

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187
Q

mismatch repair protein

A

protein complexes scan the DNA for wacky hydrogen bodning and removes/replaces the nucleotide

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188
Q

abnormal hydrogen bonds

A

when a purine x purine or pyrmadine x pyramidine happens by accident

189
Q

base-pair substitutions

A

when they accidentally take the nucelotide out of the old strand instead of the new strang

190
Q

point mutation

A

a single base is changed, inserted or deleted

191
Q

tautomeric shift

A

a base temporarily forms its rare tautomer which can pair with a different base

192
Q

tautomer

A

same chemical formula with a different arrangement

193
Q

deanimation

A

loss of an amino acid group in cytosine, forming uracil which makes an incorrect base paring

194
Q

uracil

A

base in RNA that pairs with A

195
Q

spontaneous mutations

A

caused by polymerase errors or spontaeous chemical changes in bases

196
Q

induced mutations

A

caused by matagens like chemcials or radition that damage DNA

197
Q

mutagens

A

things that induce mutations likesmoking, diet, uv radition, and ionizing radition

198
Q

excision repair

A

removes damaged nucelotides and replaces them with the right ones

199
Q

direct repair

A

can be repaired directly instead of replaces, like how photolayse breaks the dimer bonds cause in thymine by uv radiation

200
Q

thymine dimers

A

adjacent thymine link together bc of UV radition

201
Q

photolayse

A

breaks the dimer bond

202
Q

silent mutations

A

do not affect protein function

203
Q

loss of function mutations

A

prevent gene transcription or produce non functional proteins

204
Q

gain of function mutatuions

A

alters the protein function

205
Q

conditional mutations

A

produce a protein that only function sunder certain env. conditions

206
Q

tyrosinase

A

mutated pigment protein that only activates in areas that are lower than body temperature which makes colder extremities that color (liek a siamese cat)

207
Q

chromosomal mutations

A

affect long DNA sequences

208
Q

deleterious

A

cause harm or damage

209
Q

chromosomal mutations

A
210
Q

chromosomal rearrangemnets

A
  1. deletion, 2. duplicaiton, transloaction, inversion
211
Q

deletion

A

a portion of a chromosome is lost and happens when the chromosom breaks in two location and regions with out a middle segemnt - could be fatal if you are missing genes

212
Q

duplication

A

a portion of a chromosome is repeated, happens when homologous chromosolmes break at diff positions, one has a deleiton and one has

213
Q

translocation

A

a portion of a chromosome is incorrectly located - when two homologous chromostomes creak and exchange segments

214
Q

inversion

A

portion of the chromosome is flipped - chromosome breaks twice and rejoins but the segment is inverted

215
Q
  1. What are mutations? And what are some of the general reasons they can occur?
A

when mistakes happen and change the DNA sequence

216
Q
  1. Compare/contrast somatic and germline mutations. Which type can be passed on to future generations? Which type impacts only an individual?
A

germline impact future generations and somatic only effects the individual

217
Q
  1. Explain how germline mutations help provide the raw material for evolution.
A

they can cause changes that may or may not be evolutionarliy useful, and if it is, then it continues to be in the population

218
Q
  1. What is the incorporation error rate? And how is DNA polymerase able to correct itself?
A

around 1 in 100,000, and they proofread and mismatch repair if need be

219
Q
  1. What happens if DNA polymerase causes a base pair mismatch and doesn’t catch its mistake?
A

becomes a point mutation

220
Q
  1. What are the two ways that mismatch repair proteins can make a mistake? What are the results of each of these mistakes?
A

remove the nucleotide and replace it - can accidentally remove the wrong nucelotide

221
Q
  1. Compare/contrast the two ways that bases themselves can be altered in a way that causes them to be paired with the incorrect base.
A

tautomeric shift - base forms its rare tautomer that causes it to pair wiht the wrong base vs deamination where it C looses an amino acid and accidentally becomes a uracil

222
Q
  1. What is the difference between spontaneous and induced mutations?
A

spontaneous happes bc of lil errors by the polymerase or by the chemical changes, where as induced mutaions are caused by mutagens

223
Q
  1. What is a mutagen? List examples of chemical and radiative mutagens.
A

smoking, diet, uv radition, nucelar bombs

224
Q
  1. What are the two ways that damaged DNA can be repaired? How does each work?
A

excision repair - removed the damged nucleotides and replaces them
direct repair - directly repairs the nucelotide (thymine dimer example)

225
Q
  1. How do mutations impact cells? List and describe the four types of mutations based on their impacts on the proteins that result. How does each of these impact the phenotype of an organism with these mutations?
A

silent - doesnt do anything
loss of function - nonfunctional proteins
gain of function - altered fucntion

226
Q
  1. Explain how a kitten might have point coloration when that allele is not in the population’s gene pool. What type of mutation is this? (Somatic vs Germline, Spontaneous vs Induced, Silent vs loss of function vs gain of function vs conditional) Describe how the mutation that causes point coloration impacts the protein and phenotype.
A

somatic, spontaneous, conditional

227
Q
  1. List and describe each form of chromosomal rearrangement (Deletion, Duplication, Translocation, and Inversion. What situations cause each to occur?
A

deletion - portion ofo chromosome is lot
duplication - portion is repeated (break at diff points)
translocation - incorrectly located (break and exchange segments
inversions - portion of a chromosome is flipped

228
Q
  1. Which type of mutation is more likely to be deleterious (harmful): a point mutation or a chromosomal mutation? Why?
A

chromosomal because more stuff can get messed up

229
Q

Mc1R gene

A

melanocortin 1 receptor protein on melanocytes

230
Q

eumelanin

A

brown/black pigment

231
Q

pheomelanin

A

red/blond pigment (mutant mc1r causes red hair)

232
Q

archibald garrod

A

hypothesized that genes encode enzymes

233
Q

alkaptonuria

A

black urine diesase, caused by accumulation of homogentistic acid with recessive inheritance pattern - the non functional enzyme for not being about to break down the acid was inherited genetically

234
Q

homogentisic acid

A

acid that accumlates in urine in alkaptonuria

235
Q

beadle and tatum

A

developed a method for studying mutations taht ‘knock out metabolic pathways

236
Q

“knock out” mutation

A

mutation that stops the gene that encodes for arginine

237
Q

polypeptide

A

part of a protien

238
Q

hemoglobin

A

single protein made of 4 polypeptide chains

239
Q

central dogma of molecular biology

A

info flows from DNa to RNA to polypeptide (protein)

240
Q

messenger RNA

A

contains info to build polypeptides (gives instructions)

241
Q

ribsomal RNa

A

builds the amino acid chain

242
Q

transport RNA

A

brings the next amino acid to add to growing polypeptide (ikea example)

243
Q

gene expression

A

involves the transcription and translation of mRNA

244
Q

rNTPs

A

add nucelotides to RNA

245
Q

dNTPs

A

add nucelotides to DNA

246
Q

promoter

A

sequence of DNA that tells where to start transcription

247
Q

ribose

A

used instead of deoxyribose

248
Q

exon

A

coding regions that are translated into polypeptides

249
Q

intron

A

removed from pre mRNA and exons are put together

250
Q

hybridization experiments

A

denatured DNA will hybridize with homologous single stranded RNA or DNA

251
Q

RNA splicing

A

removing introns and splicing intron

252
Q

consensus sequences

A

short sequences between exons and introns

253
Q

snRNPs

A

small nucelar ribonuceloprotein particles

254
Q

spliceosome

A

composed of snRNPs and additional proteins

255
Q

branch site

A

location on intron where 5’ end joins to form loop

256
Q

5’ cap (G caps)

A

cap added ot the 5’ end, facilitates to the ribosome and prevents digestion by ribonucelases

257
Q

Poly A tail

A

added to the 3’ end, helps RNA leave the nucleus and contributes to the dtability

258
Q

Explain how genes are expressed to produce phenotypes. What do genes encode for?
How does that produce a phenotype? (Think about the red hair allele as an example.)

A

each gene encodes for a polypeptides which influences phenotypes - ex. a mutation in the gene for red hair (MCR1) can make it so that the polypeptides formed cause the hair to be red

259
Q

Explain how Archibald Garrod’s research involving alkaptonuria led to his hypothesis
that genes encode proteins.

A

he studied the black pee (alkaptonuria) and realized that it was probably because a non -fucntional enxqyme that could not break down homogenisitic acid

260
Q

Explain Beadle & Tatum’s experiment. How did they knock out the metabolic pathway for
the production of arginine? How did this support the idea that genes encode enzymes?

A

they made bread spores, moved them into tubes and put them in minimal medium, and the ones that didnt grow (the defectivce ones) were put in different tubes with one other nutrient, and they foudn arginine helped it grow, meaning hte enzyme that encoded for arginine was non functional

261
Q

What were the two discoveries made that changed the “One gene–one enzyme”
hypothesis to the “One gene–one polypeptide” hypothesis?

A

genes can encode for proteins other an enxyme and some proteins are made of multiple polypeptides

262
Q

Explain the central dogma of molecular biology. How is genetic information expressed?
Describe the flow of the information, how it is transformed, and what processes
transform it

A

dna to RNa ro polypeptide, DNA to RNA is transcription and RNA to plypeptide is translation

263
Q

Describe the three main products of transcription and explain how they work together to
form polypeptides. What parts does each play in this process? Which one contains the
information being expressed?

A

mRNa, rRNA, tRNA - mRNA reads the instructions, rRna builds the chain, and tRNA supplies the bases/materials

264
Q

Describe the overall process of gene expression with relation to the processes involved
and where these processes occur within a cell.

A

template DNA is transcribed into mRNA and it is processed and moves out of the cytosol (nucleus ) and then it is translated to a polypeptide

265
Q

Compare/contrast transcription and DNA replication.

A

transcription is from DNA to RNA, where are replication is DNA to DNA, also RNA is single stranded

266
Q

Explain what happens during each step of transcription: initiation, elongation, and
termination.

A

initiation - binds to promoter
elongation - one strange with a ribose backone
termination - recognizes termination sequence na dseperates the RNA from the DNA template

267
Q

Why is it much more acceptable for mutations (misplaced nucleotides by RNA
polymerase) to occur during transcription when compared to DNA replication?

A

RNA sequences are short, errors arent passed on to offspring and many RNA have a short life span

268
Q

In what ways is mRNA (Pre-mRNA) processed after transcription to create mature
mRNA that is ready for translation? What sequences are removed? What is added to
each end

A

introns are removed, 5’ cap is added and 3’ poly A tail is added

269
Q

Explain the differences between introns and exons, and how hybridization experiments
discovered introns. Why did a loop form in the DNA during the hybridization of mature
mRNA, but not during the hybridization of Pre-mRNA?

A

introns leave, exons stay - they found out bc the mRNa ould hybridize with the denatured DNA and it wouldn’t connect with the introns which let to them creating lil loops

270
Q

Describe the process of RNA splicing. Explain how each of the components (consensus
sequences, snRNPs, spliceosome, and the branch site) are involved in the process of
removing introns

A

snRNPs bind near consensus sequences, and then the splicesome removes the intron by cutting 5’ end of intron and attacing it to branch site and cutting 3’ end to research intron and then splices the two exons together

271
Q

What are the 5′ cap (G cap) and Poly A tail? What are their functions for the mature
mRNA molecule?

A

5’ cap is the beginning, it facilitaties binding to the ribsome and prevents digestion by ribonucleases
the Poly A tail is at the end and ithelps the mRNA leave the nucleus and helps with stability

272
Q

Codon

A

genetic information that is chunked into 3 letter sequences

273
Q

Nirenberg and Matthaei

A

discovered the first codons through experiments involving synthetic mRNA

274
Q

Poly-U

A

made a chain on U which is straight phenylalanine

275
Q

Radioactive phenylalanine

A

what was used to measure the radioactivity of the poteins porduced using different lengths of poly u

276
Q

sense codon

A

61 code for amino acids, makes sense and encodes a protein

277
Q

nonsense codon (stop codon)

A

terminate translation

278
Q

start codon

A

starts translation

279
Q

degenerate genetic code

A

each amino acid had 2-6 codons

280
Q

transgenic organism

A

genes can be inserted into another organism and function

281
Q

synonymous mutations

A

dont alter the amino acid

282
Q

missense mutation

A

change the amino acid sequence

283
Q

nonsense stop mutation

A

produce a premature stop codon

284
Q

loss-of-stop mutatuion

A

change a stop codon to a sense codon and then the polypeptide

285
Q

frame-shift mutation

A

insertions or deletions of one or more bases (not multiples of 3) ususally ends with a loss of function

286
Q

amino acid attachment site

A

tRNA binds to a specific amino acid

287
Q

anticodon

A

nucleotide triplet that is complementaaryt to the mRNA codon for the attached amino acid

288
Q

wobble

A

third base of a codon does not always need ot match the anticodon (wobble room)

289
Q

ribosome

A

consists fo the large subunit and the small subunit

290
Q

large subunit

A

3 RNA
binding sites - APE

291
Q

small subunit

A

validates the match of mRNA codon to tRNA anticodon

292
Q

a (amino acid) site

A

tRNA binds to codon of mRNA

293
Q

P (polypeptide) site

A

tRNA adds amino acid to polypeptide chain

294
Q

E (exit) site

A

tRNA waits here until released from ribosome

295
Q

Initiation complex

A

forms when small subunit binds to mRNA and locates the start codon

296
Q

Protein release factor

A

binds and breaks bodn between polypeptide chain and tRNA

297
Q

polyribsome/polysome

A

strand of mRNA with its associated probsomes

298
Q

signal sequences

A

tells proteins where to go

299
Q

RER (rough endoplasmic reticulm

A

RER signal sequence stops translation until ribosome at RER

300
Q

phosphorylation

A

addition of phosphate groups, chaning the shape (function)

301
Q

glycosylation

A

addition of carbs to form glycoproteins, which have many important functions

302
Q

proteolysis

A

cutting long polypeptides into smaller pieces that have thier own function or removal of signal sequences

303
Q

How does genetic information contained in mRNA encode for specific amino acids?

A

mRNA has codons which are then translated into polypeptides by going through the rough ER

304
Q

Why do codons exist, and how were they discovered?

A

codons exist to code form specific amino acids, and were discovered by nirenberg and mathaei with the poly U experiemnt with synthetic mRNA

305
Q

What patterns do you see when you look at the table of all amino acids? Can multiple
codons encode from one amino acid? Can one codon encode multiple amino acids? What can you infer about the code based onthese answers?

A

multiple codons can encode for one amino acid, but a codon cannot encode for multiple amino acids

306
Q

Describe what is meant by the genetic code being degenerate.

A

many codons can code for a singe amino acid

307
Q

Compare/contrast start and stop codons

A

start codon is an actual amino acid, where as the stop codon is nonsense

308
Q

Compare/contrast sense/missense (stop) codons.

A

sense - codes an amino acid, missense/nonsense, do not code for an amino acid

309
Q

What does it mean that the genetic code is universal? What are the implications of this?

A

all organisms use the same codons to encode the same amino acids - shows that genetic code is ancient and that genes from one organism can be inserted into another and still function.

310
Q

Describe what is meant by a transgenic organism.

A

genes from one organism can be inserted inota nother and function

311
Q

Explain how each type of mutation impacts the chain of amino acids produced:
synonymous, missense, nonsense (stop), loss-of-stop, and frame-shift

A

synonymous - literally does nothing bc they mean the same thing
missense - changes it to another amino acid, concerning especially if its methionine
nonsense - prematurely stops the process
loss -of-stop - keeps on going by accident
frame-shift - insertion or deletion of not 3 codons, which causes all the amino acids to be off

312
Q

What are the two major sites on a tRNA molecule, and what is the function of each?

A

amino acid site (binds to a specific amino acid) and anticodon (nucleotide triplet complemtary to the mRNA codon for the attached amino acid

313
Q

Explain the concept of “wobble” in reference to codons. What does this allow

A

wobble means that the third base of a codon does not always needd ot match the anticodon, which allows fewer tRNA variants while avoiding ambiguity.

314
Q

Describe all of the major parts of a ribosome: large subunit, small subunit, A site, P site,
and E site

A

large subunit has the 3 tRNA binding sites, APE, and a small subunit which validates the match of the mRNA codon to tRNA anticodon. A is where the tRNA binds to the codon of the mRNA, P is where tRNA adds the amino acid to polypeptie chain and E is where the tRNA waits until its released from the ribosome

315
Q

Explain the process of translation in detail. What happens during initiation, elongation,
and termination? What site do tRNA molecules bind to? What is the site where the
growing polypeptide chain is attached? Explain how termination works in translation

A

mu

316
Q

Why is it beneficial that multiple ribosomes can translate a single mRNA molecule
simultaneously?

A

much more efficient than doing it one at a time

317
Q

What helps direct polypeptides to different locations in the cell post/during translation?

A

signal sewuences

318
Q

Describe the three ways that polypeptides can be modified post-translationally. How do
each change the polypeptide, and why might each be necessary

A

phosophorylation
glycolization
proteolysis

319
Q

Gene regulation

A

allows genetically identical cells to have different phenotypes

320
Q

sonic the hedgehog gene

A

produces a protein that regulated the epression of genes involved in development throughout the body

321
Q

hox genes

A

set of genes encoding for regulatory proteins involved in specifying bodysegment identity

322
Q

inducible genes

A

not expressed unless products are needed

323
Q

repressible genes

A

usually expressed unless products are not needed

324
Q

constitutive genes

A

expressed at a constant rate

325
Q

transcription factors

A

reguatory proteins that control gene activity

326
Q

repressors

A

prevent transcription

327
Q

activators

A

stimulate transcription

328
Q

lac operon

A

inducible sries of genes that create products that break down lactose

329
Q

lactose

A

milk sugure

330
Q

trp operon

A

repressible series of genes taht create prodcutss used to synthesize tryptophan

331
Q

tryptophan

A

happy chocolate chmiecal

332
Q

operon

A

series of genes with a single promoter

333
Q

promoter

A

regulatory sequence

334
Q

operator

A

regulatory sequence between the promoter and the geense, acts as a binding site for a repressor

335
Q

negative regulation

A

repressor blocks the RNA polymerase, preventing transcription

336
Q

positive regulation

A

activators stimulate the transcription of an operon, which is positive regulation

337
Q

DNA binding site

A

where transcription factors bind to target DNA

338
Q

allosteric site

A

where other molecules can bind

339
Q

allolactose

A

inducer, binds ot the repressor where lactose is present

340
Q

inducer

A

induces the expression of the gene by binding to the repressor

341
Q

co-repressor

A

binds with the repressor to prevent gene expression

342
Q

TATA box

A
343
Q

TFIID

A

binds to the TAT box of the promoter

344
Q

general transcription facots

A
345
Q

basal transcription apparatus

A

multiple general transcriptuon facots bind, which forms the basal transcription apparatus

346
Q

specific transcription factors

A

activators

347
Q

enhancer

A
348
Q

silencer

A
349
Q

cell differentiation

A
350
Q

epigenetics

A

chemcial modification of DNA “packaging” that influence gene expression

351
Q

nucleosome

A

composed of 8 histone proteins around which DNA is wound

352
Q

histone

A

things that dna is wound around

353
Q

histone ‘tails’

A

htey have amino acid tails, therei s a strong attraction between positive histone tails and negative phosphate groups of SNA

354
Q

acetlyation

A

addition of acetyl gorups to the end of histone tails, neutralizing thier charges and opening up condesnsed DNA

355
Q

histone acetyltransferases

A

add acetyl grouds, allowing transcription

356
Q

histone deacetylases

A

remove acetyl groups, repressing transcription

357
Q

methylation

A

adding methyl groups to cytosine bases in DNa whic represses transcription

358
Q

DNA methyltranderase

A

catalyzes modification f cytosines into 5-methylcytosine

359
Q

Demethylase

A

catalyzing removal of methyl groups from cytosien

360
Q

5-methylcytosine

A

binds to proteins involved in repression of transcription

361
Q

CpG islands

A

regions rich in C and G which stop transcription if methylated

362
Q

Hemimethylated

A

half is methylated bc of semiconsverative replication

363
Q

Euchromatin

A

diffuse and light-staining; unmethylated (genes can be expressed)

364
Q

Heterochromatin

A

condensed, dark-staining, methylated (genes are silenced)

365
Q

Barr Body

A

either X in female mammals can be methylated/silences

366
Q

monozygotic (identitcal) twins

A

3 yo identical twisn have nearly identical methylation patters, but 60 yo twins hte pattern may be very different

367
Q

alternative splicing

A

differnt combos of exons are spliced toether to create differnt mRNas

368
Q

MicroRNAs (miRNAs)

A

bind to mRNA to block translation or cause premature degradation

369
Q

translational repressors

A

proteins bind to mRNas to prevent translation

370
Q

ubiquitin

A

protein that identitfies other proteins for breakdown by the proteasome

371
Q

proteasome

A
372
Q

cell division

A

one mother cell gives rise to two daughter cells

373
Q

reproduction

A

organisms pass genetic infor to offsprint through cell division

374
Q

growth

A

increasing number of cells in eukaryotes

375
Q

regeneration

A

regrowth of cells/tissues in eukaryotes

376
Q

asexual reproduction

A

directly produces offspring that are clones. of the parent organism

377
Q

sexual reproduction

A

produces gametes that are then fused together through fertilization to produce offspring with genetic variation

378
Q

binary fission

A

prokaryotes

379
Q

mitosis

A

eukaryotes, both unicelluar(like yeast) and multicellular (aspen trees)

380
Q

mutations

A

only way asexual reproduction produces genetic variation

381
Q

meiosis

A

eukaryotes only! 2 rounds of cell division to produce gametes

382
Q

fertilization

A

fusion of two gametes produced via meiosis

383
Q

gametes

A

sex cells with half the amount of chromosomes

384
Q

haploid

A

gamete, half the chromosomes

385
Q

diploid

A

somatic cell, all the chromosomes

386
Q

zygote

A

product of fertilization

387
Q

cell division signals

A

initiate cell divison

388
Q

DNA replications

A

creates. acopy of cell’s genetic info

389
Q

DNA segregation

A

distributes copies of DNA into two new cells

390
Q

cytokinesis

A

divison of cytoplasm to form two new cells

391
Q

ori (origin) site

A

start of the dna in a prokaryote (because. itis circular)

392
Q

nuclear envelope

A

membrane around hte nucleus that protects DNA

393
Q

centrosomes

A

chillinuntil mitosis or meiosis when it has to create spindles. topull apart chromatids

394
Q

chromosomes

A

condense and hold genetic material

395
Q

cell cycle

A

has two phases, interphase and m phase

396
Q

interphase

A

G1 phase, S phase (DNA syntheis, DNA is replicated) , G2 phase

397
Q

M phase

A

mitosis and cytokinesis

398
Q

g1 phase

A

gap 1, cells carry out normal functions

399
Q

g0 phase

A

resting phase outside of the cell cycle

400
Q

S phase

A

DNA is replicated

401
Q

g2 phase

A

cell prepares for mitosis, DNA is checked for errors

402
Q

prophase

A

condensation of chromosomes, spindle assembly begins, chromin coils and creates chromosomes, kinetochores form at the centromere and centrosomes move toward poles. andproduce long protein fibers called microtubiles which form a spindle

403
Q

prometaphase

A

nuclear envelope breaks down, chromosomes attach to the spindle

404
Q

metaphase

A

alignment of chromosomes along the equatorial plane

405
Q

anaphase

A

seperation of chromatids; migration to poles

406
Q

telophase

A

chromosomes decondense; nuclear envelope re-forms

407
Q

chromatin

A

uncondensed chromatid

408
Q

kinetochore

A
409
Q

centromeres

A

attach the chromatids together

410
Q

sister chromatids

A

2 of the same chromatids

411
Q

microtubule

A

long protein fibers that create the spindle

412
Q

spindle

A

made of microtubules and move the chromatids to the pole

413
Q

equatorial metaphase plate

A

line down the middle of the cell

414
Q

contractile ring

A

ring made of actin to sinch and seperate the cells

415
Q

actin

A

structual protein in the cell

416
Q

cell plate

A

in plants, used to sepereate the cytoplasm

417
Q
  1. What processes is cell division necessary for? And what do they each do?
A

reproduction (create new organisms), growth (add more cells to a multlicelluar organism and regeneration (re grow damaged tissues and cells)

418
Q
  1. How do asexual and sexual reproduction differ? Describe each process.
A

asexual - only one organism, and its genetically identitcal, sexual - 2 organisms gametes fuse together

419
Q
  1. Describe the two forms of cell division that are used in asexual reproduction. Which groups of organisms use each?
A

binary fission - prokaryotes, mitosis - eukaryotes

420
Q
  1. Describe the general series of events that occur during cell division.
A

the dna is condensed into chromatin, and condenses further into chromatids. centrosomes form a spindle fiber made of microtubules, and then the nuclear envelope disintegrtes. The chromosomes line up on the equatorial plate and then the spindes attach tot them and pull them apart so they break in hald. Then, the cleavage is forme dna the contractile ring splits the two cells, and. thenucelar envelope re forms

421
Q
  1. Describe the process of binary fission. Which organisms use this process?
A

prokaryotes

422
Q
  1. Describe what happens to the: cell membrane, nuclear envelope, centrosomes, and chromosomes during cell division
A
423
Q
  1. List and describe the phases and sub-phases of the eukaryotic cell cycle.
A

Interphase ((g0)G1, S, G2) and M phase (PPMAT)

424
Q
  1. Describe the important things that happen during interphase and mitosis (general).
A

s phase - DNa is replicatied , g1 and g2 ar e prepatory phses, and in M phase the cells are replicated

425
Q

homologous chromosomes

A

a pair of homologous chromosomes, one inherited from each parent

426
Q

replicated chromosomes

A

after S phase, chromosomes have 2 identitical copies of one chromosome, each called sister chromatids, (whem counting chromosomes, count centromeres)

427
Q

tetrads

A

homolougours chromosomes pair to form tetrads ‘’,,’’,,

428
Q

crossing over

A

when chromosomes cross over and produce genentic diversity

429
Q

chiasmata

A

points of crossing over

430
Q

genetic recombination

A

rearragnement of DNa sequences by breaking and rejoing chromosome segments

431
Q

reduction division

A

four genetically distinct haploud (n) cells called gametes chromosome number ishald

432
Q

aneuploidy

A

an abnormal number of chromosomes in a cell

433
Q

nondisjunction

A

chromosome pair fials to seperate at anaphase

434
Q

monosomic

A

missing a chromosome

435
Q

trisomic

A

extra chromosomsme

436
Q

trisomy 21

A

down syndrome

437
Q

karyotype

A

chromsome map

438
Q

polyploidy

A

organisms with triploid, tetraploid, or even high er numberes ( failure of the spindle to form, failure of cytokinesis, polyspermy)

439
Q

triploid

A

3n

440
Q

tetraploid

A

4n

441
Q

polyspermy

A

more than one sperm fertilizes the egg

442
Q

cell cycle checkpoints

A

g1 checkpoint, s checkpoint, g2 checkpoint, and M checkpoint

443
Q

cyclin dependent kinases (CDKs)

A

activated by binding to cyclin, phosphorylate proteins that reulare thes checkpoints

444
Q

Cyclin

A

synthesized when the cell recives signals that it can pass through that checkpoint

445
Q

retinoblastoma protein

A

blocks cell cycle progression until phsophorylated

446
Q

necrosis

A

cell is damaged or starved for oxygen or nutrients - bursts, and when an organism dies, all of its cells die via necrosis

447
Q

apoptosis

A

genetically programmed cell death, used when cell is malfunctioning, infected, or no longer needed

448
Q

Hayflick limit

A

number of times a cell can divide

449
Q

stem cells

A

lacks a hayflick limit, can develop into many differnte speciallized cells

450
Q

cancer cells

A

malignant cells taht divide without restraint

451
Q
  1. Explain how meiosis and fertilization both work together to create genetically diverse offspring.
A

crossing over, gametes merging, very diverse organism

452
Q
  1. Compare/contrast mitosis and meiosis. What happens during each form of cell division? What are the products of each? What are the overall similarities and differences?
A

meiosis essentially has double and then when they get to the II versions its basiclaly mitosis

453
Q
  1. Describe the parts and genetic makeup of a single unreplicated chromosome in contrast to a homologous pair of replicated chromosomes. How many chromosomes and chromatids are present in each?
A
454
Q
  1. Describe the process of crossing over, and explain how it leads to genetic diversity in the gametes that are produced by meiosis.
A
455
Q
  1. Explain how the stages of mitosis, meiosis I, and meiosis II differ.
A
456
Q
  1. Describe how meiosis results in a reduction division
A
457
Q
  1. Describe how the chromosomal makeup of a parent cell differs from the four daughter cells produced through meiosis. Also, how do the daughter cells compare to each other?
A
458
Q
  1. Explain how nondisjunction results in aneuploidy. Explain the process and the results of this error in cell division.
A
459
Q
  1. Compare/contrast nondisjunction in anaphase of mitosis, anaphase I of meiosis, and anaphase II of meiosis.
A
460
Q
  1. Describe the resulting karyotype of a trisomic individual compared to a monosomic individual. Explain what type of gametes were fused to produce each.
A
461
Q
  1. Describe polyploidy and explain the types of errors in cell division and fertilization that can result in polyploidy.
A
462
Q
  1. Describe polyploidy and explain the types of errors in cell division and fertilization that can result in polyploidy.
A
463
Q
  1. Which groups of organisms are more commonly polyploid, and which are not?
A
464
Q
  1. Describe why the cell cycle must be regulated in unicellular organisms and contrast that with multicellular organisms.
A
465
Q
  1. Describe what the cell cycle checkpoints are generally regulating (may want to read the text bubbles on slide 27 for more specific info).
A
466
Q
  1. Explain the process of eukaryotic cell cycle regulation via CDKs, cyclins, and checkpoint proteins.
A
467
Q
  1. Compare/contrast necrosis and apoptosis. Think about the situations when each would occur.
A
468
Q
  1. Describe the Hayflick limit. Why is this beneficial?
A
469
Q
  1. What type of cells lack a Hayflick limit? Why might this be beneficial or harmful?
A
470
Q
  1. Describe the various mutations that impact cell cycle regulation that can result in unregulated cell division (which could lead to cancer).
A

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