Last Exam Bio Flashcards

1
Q

What does it mean to “express” a gene?

A

the gene is turned on and proteins are being made

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2
Q

What is allelic exclusion?

A

when one is dominant and the other isn’t expressed

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3
Q

Give an example or two of why certain genes are expressed over another.

A

-allelic exclusion
-dominance

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4
Q

What is a karyotype? What are the best phases of the cell cycle to do this?

A

condensed chromosome, prophase

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5
Q

What chromosome combinations relate to biological sex? How is allelic exclusion applied in sex chromosomes?

A

X and Y chromosomes, Y chromosome will turn off female genes from X chromosom

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6
Q

What is trisomy?

A

when there’s three chromosome

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7
Q

What is the difference between recessive and dominant genes? How is this related to allelic exclusion?

A

dominant is expressed protein, unless two recessive

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8
Q

What was Darwin’s “blending inheritance” theory? Why is it wrong?

A

dilution until clones, wrong because still so much diversity

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9
Q

What is incomplete dominance

A

when both alleles are expressed (all skin tones dominant)

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10
Q

What is the meaning of Darwin’s “survival of the fittest”? What is evolution?

A

overtime certain traits become more common because they’re better for survival

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11
Q

Who are the following, and what did they think about genetic inheritance?
A. Hippocrates
B. Jean Baptiste Lamarck
C. Charles Darwin
D. Gregor Mendel

A

A. Hippocrates
-traits are an expression of proteins, passed parent to child
B. Jean Baptiste Lamarck
-evolution, traits change over time
C. Charles Darwin
-origin of species, survival of the fittest
D. Gregor Mendel
-study of peas, “GENES” passed down from parents, DNA is different than the traits

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12
Q

Define evolution

A

when traits change over time

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13
Q

What are the two components of “survival of the fittest” and how does it relate to evolution?

A

-survive
-reproduce

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14
Q

What’s the difference between genes and traits?

A

genes- DNA
traits- proteins expressing DNA (not recessive)

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15
Q

Define purebred and hybrid

A

pure bred
-homozygous
-same allele from both parents

hybrid
-heterozygous

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16
Q

What are the P1 and F1 generations?

A

P1
-parents

F1
-first generation

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17
Q

What is a genotype? A phenotype? How does an organism’s genotype lead to certain phenotypes, keeping in mind dominant and recessive alleles?

A

genetype
-DNA

phenotype
-whats expressed

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18
Q

How does genetic dominance work with human blood types (A, B, and Rh antigens)?

A

A B and Rh are codominant, they can all be expressed together

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19
Q

What is the significance of the “independent assortment” or genes?

A

creates genetic diversity

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20
Q

how do blood cell proteins work

A

if blood cell has A B or Rh (+) proteins they will be attacked if not a match

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21
Q

What is epigenetics? Give at least one example of epigenetic expression.

A

when the environment affects gene expression, skin cells vs heart cells different by need

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22
Q

How do twin studies help us understand epigenetics?

A

they have the same DNA but can still look different

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23
Q

What is the job of the enzymes Mut S, Mut L, and Mut H?

A

work together the check if double helix is smooth (bump = mismatched bases)

mut s- finds mismatch
mut l- connects them
mut h- cuts nucleotide so it can be fixed

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24
Q

What is the function of DNA polymerase?

A

-protein that copies DNA, fixes its own mistake, used for DNA replication
USED IN PCR

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25
Q

Describe how our cells develop mutation. Describe how our cells can correct DNA mutations.

A

when a base is copied wrong, muts slh

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26
Q

6 types of mutations

A

silent (synonymous)
-DNA change, dif base same codon

missense (nonsynonymous)
-DNA change, codon/AA change

stop (nonsense)
-stop codon added

frameshift
-adding or removing base, shifts other bases over (new groups of three)

germline
-gametes have mutation

somatic
-cancer, WBC kill messed up cells

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27
Q

What is a restriction enzyme/endonuclease? Can you recognize where a given enzyme will cut given a diagram?

A

-it cuts DNA a certain way (uneven two strands)

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28
Q

blunt vs sticky end? How are they useful for manipulating DNA?

A

blunt
-even cut

sticky
-uneven cut
-allows DNA to get inserted into the sequence

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29
Q

whats PCR

A

polymerase chain reaction
-makes a ton of DNA

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30
Q
  1. Name the protein that can convert RNA into DNA.
A

reverse transcriptase

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31
Q
  1. Why would we want to extract mRNA from a cell and turn it into DNA for PCR?
A

you dont wanna take DNA out of a cell

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32
Q
  1. What kinds of nucleic acid can a virus use for its genome?
A

-both RNA and DNA

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33
Q
  1. What is a capsid made of?
A

protein

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34
Q
  1. Why would an RNA virus use reverse transcriptase?
A

to make DNA in order to replicate

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35
Q
  1. What does RT-PCR stand for? Why do we do it?
A

reverse transcriptase polymerase chain reaction
-to turn RNA -> DNA, and make more DNA

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36
Q
  1. List the “ingredients” needed to run PCR.
A

-DNA
-DNA polymerase (taq polymerase)
-nucleotides: AGTC
-buffer: liquid with salt at a pH
-primer: small piece of DNA (forward and reverse primer)

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37
Q
  1. What does a buffer do in PCR
A

maintains pH to prevent denaturing of Taq Polymerase

38
Q
  1. To what strand does the Forward Primer bind? To what strand does the Reverse Primer bind?
A

Reverse primer
-binds to positive strand

Forward primer
-binds to negative strand

39
Q
  1. Know the steps of the PCR cycle.
A

denaturation (hottest)
-split strands

annealing (coldest)
-primers hop on

elongation
-taq polymerase reads 5’ to 3’ and makes other strand (top is opposite of reading direction)

40
Q
  1. What do we use PCR for? what do we use gel electrophorysis for
A

-to copy tons of DNA

-to make sure experiment correct, or match DNA

41
Q
  1. What is a tandem repeat?
A

two of the same sequence right next to eachother

42
Q
  1. How does gel electrophoresis differentiate between sequences that have different numbers of tandem repeats?
A

more repeats, longer, shorter distance

43
Q
  1. What is the study of Population Genetics?
A

study of percentages of items in population

44
Q
  1. What is evolution? What is a way we can observe bacterial evolution in a lab?
A

see which are resistance to antibiotics

45
Q
  1. How do we report a frequency? Do we have to report it even if it is 0?
A

fraction yes

46
Q

different types of natural selection (survival of the fittest)

A

stabilizing
-a trend toward the average instead of the extremes

directional
-one extreme is the best

disruptive
-either extreme is better than middle

47
Q
  1. Describe the difference between infectious disease and genetic disease.
A

infectious- caused by pathogen/microbe

genetic- caused by mutations

48
Q
  1. Define somatic mutation and germline mutation.
A

somatic- regular cells, not passed down

germline- mutations in reproductive cells and can be passed down

49
Q
  1. What are the 4 types of pathogens that can cause disease?
A

prokaryotic
-bacteria

viruses

eukaryotic
-parasite (just one cell)
-fungi=yeast=mold

50
Q
  1. What is a pathogen? What is pathology?
A

pathogen- cause of disease

pathology- study of a disease

51
Q
  1. Describe the difference between infectious and contagious diseases.
A

infectious
-you can get disease (UTI)

contagious
-you can spread it (cough)

52
Q
  1. Define vector borne disease. Give an example. Is it contagious?
A

transmitted through something non human (lyme’s through ticks)

53
Q
  1. What causes a urinary tract infection? Is it contagious?
A

no, caused by bacteria

54
Q
  1. What is the difference between a prokaryote and a single-celled eukaryote?
A

prokaryotes
-no organelles
-circular DNA
-no nucleus

single-celled eukaryotes
-has organelles
-has nucleus

55
Q
  1. What are the components that a virus always has? What are a few that some have and some don’t?
A

-capsid (protein)
-nucleic material

-lipid envelope SOMETIMES

56
Q

antigen vs pathogen

A

antigen
-piece of pathogen

pathogen
-the intruder

57
Q
  1. What is the difference between Gram-positive and Gram-negative bacteria?
A

gram positive
-peptidoglycan on the outside (only one membrane)

gram negative
-peptidoglycan inside the TWO membranes

58
Q
  1. What are the two macromolecules that can make up the outer coating of a virus?
A

-protein capsid
-lipid envelope

59
Q
  1. Define macrophage (MØ)
A

a WBC that eats harmful cells
-PRRs
-cytokines

60
Q
  1. What are Pattern Recognition Receptors (PRR)? What is the response of the cell when the receptor is activated?
A

when activated, PRR tells nucleus to make cytokines

61
Q

what are scavenger receptors

A

a kind of PRR on Macrophages that look for dead cell tissue to bring it in and digest it

62
Q
  1. What are cytokines? When are they released?
A

protein that travel between WBCs for signaling (macrophages)

63
Q
  1. How are lysosomes in MØ special?
A

they have more than just digestive enzymes, they have extra for killing pathogens

64
Q

Innate vs Adaptive Immune System

A

Innate
-1st response
-limited
-same response time
-MO, skin, mucus, PRRS

Adaptive
-2nd response (when innate needs backup)
-specific
-gets faster each time
-B & T cells, antibodies

65
Q

describe how innate triggers help from adapive

A

-macrophage brings antigen to thymus/lymph node/other
-Tₕ release cytokines to command
-T꜀ prepare to attack

66
Q
  1. Explain how the skin, stomach acid, and the mucociliary escalator work to prevent infection.
A

skin
-physical barrier

mucociliary escalator
-redirects infection to exit either (cough or digest w acid)

67
Q

cells of innate immunity

A

Macrophages (phagocytosis)

Polymorphonuclear cells (PMNs)
-Granulocytes (multi-lobe, granules)
—Neutrophils (common, first responder to infection) (phagocytosis & granules)
—Eosinophil (anti-parasite) (only granules)
—Basophil (rare, allergic response) (only granules)

68
Q

what do different granulocytes look like

A

neutrophil
-3 lobes spread out

eosinophil (like an E but no middle)
-2 lobes spread

basophil (like a B)
-2 lobes attached

69
Q
  1. How does a macrophage kill? how does a granulocyte kill?
A

macrophage
-phagocytosis (eats then lysosome)

granulocytes (granules)
-little bomb for bad things

70
Q
  1. Describe the differences between acute and chronic disease. Give an example for each.
A

acute
-fast & short (1day - 2wks)
-severe symptoms (you know you’re sick)

chronic
-slow & long (3wks-forever)
-less severe (don’t always know you have it)
-MAY NOT RESOLVE

71
Q
  1. What cells correspond to the Innate immune system? What about the Adaptive immune system?
A

innate immune system
-macrophage, granulocytes

adaptive immune system
-B cells, T cells (Tₕ & T꜀)

72
Q
  1. Where do T cells and B cells mature?
A

T cells
-in the thymus

B cells
-in the bone marrow

73
Q

what is autoimmunity

A

-when your immune system mistakes your own body for a threat and starts attacking it.
-negative selection kills the cells that do this

74
Q

types of lymphocytes

A

B cell
-secrete antibodies

Tₕ cell (helper)
-binds with macrophage on MHC II
-coreceptor CD4
-helps activate other WBC

T꜀ cell (cytotoxic cells)
-antigen in MHC I
-coreceptor CD8
-kills infected cells
-makes effector and memory cells

75
Q

what is a BCR (B cell receptor)

A

an antibody in the membrane

76
Q

what does a B effector cell do

A

make tons of antibodies in the ER

77
Q

What does it mean for a macrophage to present on MHC I vs MHC II

A

MHC I means it’s infected

MHC II means it ate the infected cell

78
Q
  1. How does a Tc know a cell is infected? How does it kill the infected cell?
A

-when a not self antigen is detected on MHC I
-point mutations till it has TCR that perfectly recognizes antigen (also makes effector and memory cells)
-releases cytokines which trigger apoptosis in infected cell

79
Q
  1. Describe the difference between effector T cells and memory T cells.
A

effector T cells
-the fighters

memory T cells
-linger for later fights

80
Q

leukocytes vs lymphocytes

A

leukocytes
-all WBC

lymphocytes
-B & T cells

81
Q

why are B and T cells “lymphocytes”

A

they mainly travel in the lymph nodes

82
Q
  1. Which cells make antibodies? What are the two kinds of antibodies?
A

B cells make antibodies
-secreted antibodies
-membrane-bound antibodies

83
Q
  1. Diagram an antibody: FAb , FC (what is the purpose of each)
A

FAb
-varies (specific to antigen)
-antigen bind side

Fc
-constant
-binds to immune cells (virus covered in antigens gets attached to macrophage)

84
Q
  1. What is “customized” during B and T cell maturation? Why is this important?
A

antigen receptors are customized so they can successfully combat different antigens

85
Q
  1. What are the 4 things antibodies can do to fight against pathogens? Give a simple diagram/explanation for each.
A
  1. agglutination
    -antibodies and viruses get all stuck together to they can’t infect the cell
  2. activate c’ proteins (parasites & bacteria)
    -antibody attaches to surface protein
    -binded c’ protein pokes hole in membrane
  3. opsonize antigens
    -antibody on virus makes it easier for FcReceptor on macrophage to grab it for phagocytosis
  4. neutralizing antibodies
    -antibodies bind to virus, dig in, and break it up
86
Q

4 kinds of vaccines

A
  1. live - attenuated
    -real virus -> can reproduce
    -less pathogenic (weaker)
  2. killed/inactivated
    -whole virus but DEAD -> no reproduction
  3. RNA
    -small nanoparticle fuses and releases RNA into cell that becomes surface protein
  4. subunit
    -piece of something
    -pray it gets picked up
87
Q

hematopoiesis

A

-the creation of new red blood cells

88
Q

Dr. Robison:
1. What disease does Yersinia pestis cause?
2. What is the purpose of wearing two pairs of gloves?
3. What did it mean when Dr. Robison talked about the suit’s “positive pressure”? Why is that important?

A

-the black plague
-creates s seal (bacteria can’t get in)
-pathogens would have to get up the suit, which is pushing pressure down the suit

89
Q

Dr. Johnson:
1. What happens to protein expression when a promoter is wrapped up in a nucleosome?
2. How do acetylation and methylation of the nucleosomes affect protein expression?
3. What is genome metagene analysis?

A

-it can’t be copied or expressed
-acetylation turns it on, methylation turns it off
-looking at DNA and seeing where the histones are bound, acetylation/methylation, analyze

90
Q

Dr. O’Neill:
1. What is immunotherapy?
2. What is a macrophage?
3. How does cancer develop?

A

-treatment using the immune system
-WBC…
-mutations…