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Genetics Flashcards

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AP® Biology flashcards Biology 101 flashcards
1
Q

Who first discovered chromatin?

A

Miescher first isolated nulcein which is now called chromatin.

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2
Q

Who discovered how bacterium can “transform”?

A

Fred Griffith tried to develop a vaccine against pneumonia and while he was studying the disease-causing bacterium he administered a pathogenic and non-pathogenic type into mice. He saw that bacterium can transform via their DNA.

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3
Q

What did Herschey-Chase show in their experiment?

A

They discovered that DNA was the “heritable material” (as opposed to protein)

  • They began this because they new that viruses infect bacteria (they are known as bacteriophages) and that viruses are composed almost primarily of DNA, protein, and insulating coat.
  • So then radioactively tagged protein and DNA in a bacteriophage and let it inject its hereditable material into a bacterium, centrifuged it, and found the bacteria at bottom with labelled DNA component, and labelled protein component on top (not in bacteria) demonstrating that DNA is in fact the heritable material
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4
Q

What did Rosalind Franklin discover?

A

She used x-ray crystallography to show the helical structure of DNA.

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5
Q

How did Watson and Crick lead off from Franklin’s discovery? What were their major conclusions?

A

They discovered that is a purine and a pyrimidine are bound together it fits within the diameter of the helical structure observed by Franklin’s experiment.
Major conclusions:
1. DNA is a double stranded molecule
2. DNA strands are complimentary (Adenosine with thymine) (cytosine with guanine)
3. DNA strands are anti-parallel (one if 5’ to 3’, other is reverse, they are held together in opposite directions)

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6
Q

How many bonds does adenine form with thymine?

A

They share 2 hydrogen bonds that hold the two strands together

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7
Q

How many bonds does cytosine form with guanine?

A

They have 3 hydrogen bonds that hold the two strands together.

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8
Q

What are the components of a single nucleotide?

A
  1. A deoxyribose/ribose sugar
  2. Phosphate at 5’ carbon on sugar
  3. Nitrogenous base at 3’ carbon on sugar
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9
Q

What is the difference between deoxyribose and ribose sugar?

A

A ribose has a hydroxyl group on the 2’ carbon, deoxyribose only has a hydrogen attached.

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10
Q

What are the differences between DNA and RNA

A
  1. They differ in the sugar (ribose for RNA, deoxyribose for DNA)
  2. RNA has uracil where DNA has thymine nitrogenous base
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11
Q

What is the type of bond that hold the nucleotide bases together in the same strand?

A

Covalent phosphodiester bonds.

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12
Q

What are Chargaff’s two rules?

A
  1. DNA % of bases varries among species (the typical ratios)

2. The % of complimentary base pairs are about equal (i.e. % of adenine is about= to the % of thymine).

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13
Q

What work did Melson and Stahl do? What were the opposing theories of their discovery?

A

They determined that DNA replication is semi-conservative (meaning that each new daughter DNA has one strand from the parent).
The other models include: conservative and dispersive/

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14
Q

In which direction does DNA polymerase work? What “problem” does that pose for DNA replication?

A

DNA polymerase works in the 5’ to 3’ direction (reads 3’ to 5’) so for the one leading strand it can complete a continuous process of replication. The other strand, the lagging strand, is opening in such a way the DNA polymerase would need to work in 3’ to 5’, so it has to continuously make a section (okazaki fragment) of replication, and then go back and work on a new part of the DNA that was recently exposed in the fork.

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15
Q

What are the enzymes that aid in the transcribing of the lagging strand?

A
  • DNA polymerase transcribes it
  • Primase lays down a small portion of RNA primer so DNA polymerase can go back and attacth and make that new fragement
  • DNA ligase joins the okazaki fragments
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16
Q

What helps unwind and keep DNA unwound during transcription process?

A

Helices unwinds the DNA, and SSBs (single stranded binding molecules) stabilize the unwound DNA.

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17
Q

Explain how there is redundancy in the genetic code but not ambiguity.

A

There is redundancy because there are multiple codons that can code for 1 specific amino acid (meaning small changes in nucleotide sequence can still produce the same protein).
There is no ambiguity because 1 codon cannot code for more than 1 amino acid, it corresponds to only 1.

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18
Q

Briefly describe the initiation stage of transcription.

A

After RNA polymerase binds to the promoter region, it pries the two strands apart and RNA polymerase will initiate RNA synthesis based on the template strand (not that this new RNA strand will be identical to other strand of DNA and is therefore called the coding strand).

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19
Q

Briefly describe the elongation process of transcription.

A

RNA polyermase moves downstream (downsream a transcription unit: promoter to terminator) making transcript in 5’ to 3’ direction, DNA helix reforms behind it.

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20
Q

Breifly describe the termination stage of transcription.

A

RNA polymerase detaches, RNA molecule released, DNA is completely re-wound.

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21
Q

What is the promoter region of a DNA molecule?

A

It is found before a gene(s) of interest where RNA polymerase can recognize and bind to. It is typically in the form of what is known as the “TATA box”
-Note that this promoter region is NOT transcribed

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22
Q

What composes the transcription initiation complex?

A

-The transcription factors bound to the promoter with the RNA polymerase bound as well.

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23
Q

What is the termination sequence in eukaryotes?

A

After RNA polymerase reaches a specific region it will transcribe a sequence of RNA known as a polyadenylation signal sequence, in which produces that signal to stop RNA polymerase from transcribing and to detach.
-Note that this is transcribed into the mRNA (but not translated)

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24
Q

What are the 5’ and 3’ ends of the mRNA? What are their purpose?

A

The 3’ “tail” is known as the “poly-A tail” because it it sum 250 adenosines added to the end of an mRNA molecule .
The 5’ “cap” is a modified form of guanine added to the mRNA.
These two alterations function to protect the mRNA from hydrolytic enzymes in the cell, as well as they aid in the attachment to ribosomes (specifically the 5’ cap)

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25
Q

Briefly describe the process of RNA splicing.

A

This is part of what converts pre-mRNA to functional mRNA (along with the ends that were added to it). It involves the removal of long non-coding regions withn the RNA transcript, that are intertwinced within coding sections (the genes).
The coding regions: introns
Non-coding regions: exons
-Note that the UTRs (non translatable parts of the mRNA) are an exception to exons, they are not spliced out. This included polyadenylation signal sequence.

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26
Q

What enzyme/complex is responsible for RNA splicing?

A

The spliceosome.

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27
Q

During translation, what are the structures involved in reading the mRNA?

A
  • Inside of a ribosome there are rRNA sites that allow tRNA to bind to it. tRNA are what is reposnible for reading the mRNA codons via the anticodons on the tRNA.
  • tRNA are composed of an attached amino acid at the top (that can attach to a hydroxyl group_ and an anticodon at the other end (called the anti-codon loop) that can bind to the codon of the mRNA.
28
Q

In which direction is the mRNA read in the ribosome/by the tRNA?

A

It is read via the 5’ to 3’ direction.

29
Q

Explain how the tRNA move through the sites of the ribosome in translation. In which site of the ribosome holds the growing polypeptide chain?

A

The new tRNA enters into the a-asite of the ribosome, its anticodon bonds with the codon, allowing the attachment on the growing polpeptide chain from the tRNA in the p-site to move over to the a-site and bind to the new amino acid.
The e-site is where the tRNA exits.

30
Q

How is translation signalled to stop?

A

Once the stop-codon from the mRNA is read by the anti-codon on the tRNA, a release factor enters the a-site: the polypeptide is freed and the ribosome dissembles.

31
Q

What is the start codon and what amino acid is it associated with?

A

The start codon is AUG and it corresponds to methionine.

32
Q

What is a polygenic mRNA?

A

A polygenic mRNA is one that contains multiple genes, all with the same promoter region and same operator.
The genes are said to be “coordinately controlled”

33
Q

What is the operator? What is the operon?

A
  • It can be described as the on/off switch for genes (directs RNA polymerase to begin transcribing or not), located either within a promoter, or between the promoter and the coding genes.
  • The operon is the operator, promoter, and the genes in that transcription unit
34
Q

What is a repressive operon?

A

One that is normally always turned on (RNA polymerase can always bind and transcribe) but can be repressed by the presence of a repressor (typically one produced from the production of genes in that operon).

35
Q

What controls repressors?

A
  • Repressors are produced from a regulatory genes: they are located upstream from the operon if interest, and therefore have their own promoter.
  • Regulatory genes are continuously expressed
  • Repressors are controlled in 2 ways: when they are bound to an operon to repress it, it frequently binds and unbinds to allow some activity, the second way is that most repressors are allosteric meaning they have active an inactive forms
36
Q

How are repressors changed into their active form?

A

A co-repressor is required (a ligand) to cause a conformational change in the inactive repressors to make it active.

37
Q

Briefly explain the trp operon and how it is controlled via repressors, co-repressors, and regulatory genes.

A

Tryptophan acts as a co-repressor from the trp repressor molecule. By binding to it, it changes it into its active from, allowing the trp repressor to bind to the trp operator and shut down the production of the tryptophan pathway.
- The trp operon is a repressible operon as the end product of the pathway is also the effector

38
Q

Briefly explain the lac operon, its pathway, and how it is regulated.

A
  • The lac operon codes for an enzyme that can hydrolyze lactose (beta-galactosidase).
  • The regulatory gene (lacI) located outside of lac operson codes for allosteric repressor proteins than can control the activity of the lac operon.
  • The lac repressor protein is made already active, and so the lac operon is innately inhibited. It requires an inducing molecule (ligand) to prevent the repressor from binding to the operator. This inducer for the lac repressor is an isomer of lactose, called allolactose (produced by the consumption of lactose). So the consumption of lactose promotes the breakdown of it in our bodies.
39
Q

What is the difference between inducible and repressible operons?

A

In inducible operons the substrate is the effector (the substrate has mechanisms to help itself in the body). This substrate is the one that prevents the inhibiting mechanism of the active repressor produced by the regulatory protein.
In repressible operons, one the end-products of the operons pathway is the one that will effect its production: so it a lot of it is produced, it will repress the activity of the operon because there is already a lot.

40
Q

What are the 3 possible outcomes of a substitution point mutation?

A
  1. Silent mutation- in which the substitution did not change the amino acid sequence and so has no observable effect on the phenotype.
  2. Missense mutation-in which substitution did change amino acid sequence: can have ranging effects to minimal to very severe if the amino acid sequence change was in a critical part of the protein.
  3. Non-sense mutation-in which a substitution created a pre-mature stop codon, almost always leads to nonfunctional proteins.
41
Q

What is often the result of insertion/deletion mutations?

A

It usually creates a frameshift mutation in which the reading frame of the genetic message is changed (happens when there are insertions or deletions that occur in multiples other than 3)
- Results in massive missense mutations, often followed by a nonsense mutation, almost always leading to a nonfunctional protein.

42
Q

What are the 2 ways that a cell can help make up for the errors in DNA replication before it becomes a mutation?

A
  1. DNA proofreading- carried out by DNA polymerase as it proofreads each nucleotide against its template strand once it is covalently bonded.
  2. Sometimes if DNA proofreading misses a mistake, a mis-match repair can occur which is carried out by enzymes (damage to these enzymes often results in massive mutations and cancers in a specific area of the body that the gene codes for)
43
Q

What are 2 ways chemical mutagens interact with DNA?

A
  1. Some chemical mutagens are nucleotide analouges, meaning they have similar structure to one or more nitrogenous bases and can therefore replace one in DNA
  2. They can insert themselves into DNA and distort the double helix structure
44
Q

Explain a way that a nucleotide analogue can damage DNA.

A

If the mutagen is analouge to two different nucleotides, it can behave as both, one normal to how the genetic code may be, and the other one creating a missense mutation or disrupting the structure.

45
Q

Briefly describe the DNA repair system for a spontaneous mutation occurring after DNA replication.

A

This is called a nucleotide excision repair and consists of:

  1. Enzymes to detect the damage/mistake
  2. Nuclease enzyme cutting out damaged part
  3. DNA polymerase filling in the new gap with correct base pairs
  4. DNA ligase sealing the two part back together
46
Q

What does UV radiation frequently do to the DNA in cells (specifically skin cells).

A

It can cause a thymine dimer, where thymines are paired adjacent to each other and bond to each other rather that with the opposite strand, causing a kink in the DNA structure.
This can be corrected via a nucleotide excision repair.

47
Q

Who are the “batman and robin” for retrction enzymes? What are restriction enzymes?

A

Nathal and Smith worked with restrction enzymes, which are apart of the “toolbox for genetic engineering”.
RE cut at a specifc part in the DNA (i.e. between and A and a C) and are found exclusively in bacterium.

48
Q

How do bacteria use RE and how can we as humans take advantage of them?

A

Bacterium contain a ton of RE with varying cutting sequences, and they use them to fight of viruses, not to cut their own DNA.
This is useful to humans because if we can extract these RE we can use it for many application in biotechnology. One way would be splicing together, using DNA ligase (part of toolbox for genetic engineering), two different pieces of chopped up DNA (via their sticky ends).

49
Q

Explain the process of gene cloning by using plasmids and RE.

A
  1. First you can take a plasmid, the cloning vector, and cut it using RE to make a spot to insert a new gene of interest.
  2. This gene of interest is from a different source, isolated via the same RE used to cut the plasmid
  3. The gene can be inserted into the plasmid via DNA ligase leaving you with a recombinant DNA molecule
  4. You can then return this recombinant plasmid into a bacterium, and are left with recombinant bacterium and it will continue to replicate this plasmid and pass it on to new bacterium.
50
Q

What are some possible reasons we would use recombinant DNA/bacteria?

A

If we insert genes that will help us with various things and remove the harmful parts, we can do this such as”

  1. Provide growth hormones to people
  2. Provide insulin to people
  3. Provide blood-clotting factors
  4. Provide factor 8 (kind of blood thinner)
51
Q

What are the organizations of DNA from smallest (DNA molecule) to largest?

A
  1. DNA (2 nm)
  2. Nulceosomes (DNA wrapped around histones) 10 nm
  3. Solenoid (grouping of nuelcosomes) 30nm
  4. Chromatin (looped) 300 nm
  5. Sister chromatid (700 nm)
52
Q

What are 2 things that happen in meiosis I that increase the genetic variability in gametes?

A
  1. Crossing over- occurring during metapahse 1, where homologous chromosomes swap DNA segments
  2. Random assortment-when homologous chromosomes line up randomly so that the new daughter cells have a random pick of what chromosomes they have (from the mom or the dad)
    - (note this is mom or dad in the gametes so like the grandparents in a way, the haploid gamete will be pure for that individual and then fuses with another individuals gamete)
53
Q

What are the varying degrees of dominance in phenotypes?

A
  1. Complete dominance: the heterozygote and dominant homozygote are indistinguishable
  2. Incomplete dominance: the heterozygote has an intermediate phenotype between the dominant and recessive alleles (appears as a type of blending)
  3. Co-dominance: both alleles have their phenotype characteristics present (i.e. with type AB blood, or with spots on animals).
54
Q

What does mendel refer to as hybridization?

A

The crossing or mating of 2 true breeding varieties: two different allele homozygotes.
True breeding parents=P generation, and their offspring are F1, and if the F1 self pollinate its F2 ( in terms of plants).

55
Q

What is mendel’s law of segregation?

A

Two alleles for a heritable character segregate during gamete formation, ending up in different gametes.

56
Q

What is mendels’ law of segregation?

A

Each pair of alleles segregate independently during gamete formation.

57
Q

What is a dihybrid cross? What are the ratios for it?

A

A cross between two heterozygotes based on law of independant assortment (i.e. 4 possible gametes crossed with 4 possible gametes), producing a 9:3:3:1 ratio.

58
Q

What are the classes of genetic disorders?

A
  1. Multifactoral
  2. Chromosomal
  3. Single gene
59
Q

What type of thing can multifactoral genetic disorders cause?

A
  1. Congenital malformations (i.e. clefft lip, heart defects)
  2. Cancer: some forms, have multiple causes including genetic predisposition
  3. Coronary artery disease: multiple causes including genetic predisp.
60
Q

What are some chromosome or cytogenetic disorders?

A
  1. Down syndrome-trisomy 21. incidence increase as age of mother increases
    - in down syndrome a portion of the third chromosome on 21 can translocate to chromosome 14
  2. XYY syndrome (due to nondisjunction): behavoiral difficulties, fertile
  3. XXY aka Kleinfelter Syndrome: sterile male with female body characteristics.
  4. Turner Syndrome (X): sterile female, short stature, premature sex organs
  5. XXX Syndrome: learning difficulties, fertile
61
Q

What causes a single gene disorder? What are some types?

A

Caused by a mutant gene (faulty). Can be presented either by being on only 1 chromosome of a homologous pair (dominant) or on both (recessive). Patterns can usually be observe from a pedigree.
Some example include:
1. Cystic Fibrosis: autosomal recessive disease
2. Duchenne Muscular Dystrophy: X-linked recessive disorder
3. Huntington’s disease: autosomal dominant, late onset
4. Sickle cell anemia: autosomal reccessive

62
Q

What are 3 questions a geneticist will ask about a genetic disorder?

A
  1. Is it autosomal or sex-linked?
  2. Dominant or recessive?
  3. Single or multi-gene caused?
63
Q

How can you tell from a pedigree if a disease is autosomal or sex linked?

A

If it is sex linked it will appear predominately in males.

64
Q

How can you tell if a disease/disorder causing trait is dominant or recessive from a pedigree?

A

If dominant, every affected child will have an affected parent.

65
Q

How can you tell if a disorder/disease shown on a pedigree is from a single gene, or if it is caused by multiple genes?

A

If single gene, the affected individuals should occur at a frequency of 25% (3:1 ratio) from heterozygous parents.

66
Q

What would happen if 2 traits were located on the same chromosome and a dihybrid cross was conducted?

A

They would deviate from the 9:3:3:1 ratio because they did not independently segregate.

Biology (6 decks)

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