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Genetics > Exam 4 > Flashcards

Exam 4 Flashcards

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Biology 101 flashcards
1
Q

List and describe Darwin’s four postulates of evolution

A

1: individual species are variable
2: some variation is heritable
3: individuals vary in survival and reproductive success
4: survival and reproduction are not random

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2
Q

What is the evolutionary synthesis?

A

combo of mendel and darwin’s ideas –> darwin had no concept of genetics (no alleles or chromosomes)
genes are on chromosomes
evolution = small genetic changes and natural selection

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3
Q

What are the different meanings of the word evolution from a genetics perspective?

A

change in allele frequencies over time
mutations to form new alleles
formation of new species
genetic relatedness (btwn phyla, family, etc.)
major changes in body

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4
Q

How does Darwin’s model of evolutionary change contrast with the fossil record?

A

fossil record shows that species stay (relatively) the same over time, but get replaced by other species
darwin thought species would change gradually over time
fossil record = stability
darwin = change

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5
Q

What is punctuated equilibrium and why was it proposed?

A

rapid changes followed by stasis (stable species, something happens, changes morphology suddenly)
proposed as explanation to fossil record changes

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6
Q

What was the Cambrian explosion and how does it challenge the evolutionary model?

A

sponges, cnidarians, comb jellies –> sudden explosion leads to all body plans

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7
Q

What are developmental genes and how are they involved in evolutionary change?

A

developmental “toolkit” - lay out body plans, tell cells how to form fossils, where things are going to grow, etc.
changes in body plan = location, timing, amount of protein, changes in gene expression
thought this is what caused Cambrian explosion, change in how body plans change

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8
Q

What are the critiques of Darwin’s model of evolution from a developmental biology perspective?

A

darwin believed in gradual change in morphology (anagenesis)

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9
Q

Distinguish anagenesis from cladogenesis

A

anagenesis - change within a species (gradual change in morphology) –> rare (based off fossil record)
cladogenesis - speciation (formation of new species)

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10
Q

What advantages are there to studying molecular variation?

A

no phenotypic effect
helpful for studying lineage
widely applicable
establishes genetic relatedness btwn different organisms
sequences inferred from related species
large data sets (whole genome)
quantifiable (# of changes per generation)

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11
Q

What are the two general categories of reproductive isolation?

A

prezygotic - no zygote forms, populations do not interbreed
postzygotic - zygote forms, populations interbreed but do not produce viable offspring

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12
Q

How is sympatric speciation different from allopatric speciation?

A

allopatric (“other country”) - geographic barrier prevents interbreeding (prezygotic barrier)
isolation = genetic differences –> incompatibility btwn 2 populations
sympatric (“same country”) - reproductive isolation without physical barrier

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13
Q

morphological variation v.s. molecular variation

A

morphological - genetic and environmental causes
includes fossil record
basis for selection
molecular - may or may not have phenotype
predominant basis of evolutionary studies today

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14
Q

neutral mutation hypothesis

A

variants are generally functionally equivalent (most variation on molecular level doesn’t affect fitness)

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15
Q

balancing selection

A

individual variants have selective effects, but the population favors multiple alleles (heterozygote advantage)

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16
Q

what causes sympatric speciation?

A

can occur through underdominance (heterozygote disadvantage) or positive assortative mating

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17
Q

What is a phylogeny and what are the two general ways to construct them?

A

evolutionary tree
made through taking morphological traits (including fossil records) or genetic comparisons (gene trees)

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18
Q

Taxa

A

species you’re looking at

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19
Q

Branches

A

history that leads you to taxa

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20
Q

Nodes

A

inferred common ancestor (inferred because no fossil record)

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21
Q

Root

A

common ancestor

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22
Q

Outgroup

A

related but distantly related (i.e. horses and donkey)

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23
Q

What are two guiding principles when constructing phylogenies?

A

distance approach: look at overall degree of siimilarity
principle of parsimony: what are the fewest number of changes that would need to occur between these phylogenies?

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24
Q

What are homoplasies and how do they confound phylogeny construction?

A

trait that is shared btwn taxa but NOT in a common ancestor
feature would’ve had to arisen twice

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25
Q

What is the difference between a gene phylogeny and a species phylogeny?

A

a gene tree is just a zoomed in version of a species tree

26
Q

Explain the reason for differences in nucleotide substitution rates in different parts of genes

A

matter of selection
substitution rates are the same but some regions are tolerated and some are not

27
Q

What is a molecular clock?

A

estimate of when common ancestor lived
limited application

28
Q

What is the role of gene duplication in evolutionary change?

A

gene duplication allows one copy to keep doing what its doing and another to mutate and acquire new function

29
Q

What is synteny and how is it demonstrated by comparing the sorghum and maize genomes?

A

synteny - fairly big region of chromosome that lines up from one species to another
little lines show where there is a chromosome in a common ancestor

30
Q

What is horizontal gene transfer and how does it complicate phylogeny construction?

A

transfer of genes btwn unrelated organisms (rare)
if you’re trying to find heritable connections between species, genes that come from a completely unrelated species will through off this data

31
Q

possible explanations for homoplasy?

A

convergent evolution (like flying in birds or bats)
loss of feature in other taxa (violates parsimony)
reversion, especially in DNA sequences

32
Q

What is the possible role of microRNAs in evolution?

A

increase in number in vertebrate evolution
- invertebrates (like hemichordates and sea urchins) don’t have any
- vertebrates (especially mammals) have a lot

33
Q

What are some of the functions of TP53 as it relates to cancer?

A

checks for cell damage and causes cell suicide (before cell gets to mitosis) if defective –> if cell has one good and one bad, good might mutate (leaving only bad) and then you have cancer cells
also maintains genome stability

34
Q

Describe the steps in cancer progression

A
  • unregulated cell division
  • loss of apoptosis
  • loss of cell identity (allows cell to move around/survive unidentified)
  • ability to invade surrounding tissues
  • ability to form metastases (second form of cancer)
  • loss of senescence (lose ability to divide)
35
Q

If cancer arises through genetic mutations, how does cancer arise spontaneously vs. being caused by the environment?

A

spontaneous: mutations in DNA replication
environmental: mutagens can cause cancer
most cancers are caused spontaneously, some caused environmentally, very few heritable

36
Q

Describe how viruses can be involved in cancer

A

some nonhuman retroviruses (when entered into genome, pick up a mutated version of a gene and transfer) contain genes that can cause cancer (mutated versions of cellular proto-oncogenes, picked up by transduction)

37
Q

Describe the role of tumor suppressor genes in cancer

A

regulate cell growth, inactivated in cancer
recessive mutation

38
Q

Describe the roles of Rb and E2F in cell cycle progression and cancer

A

checkpoint btwn g1 and s phase –> E2F lets cell continue on to s phase
Rb - normally binds to (and inhibits) E2F (growth-stimulating protein)
phosphate group added to Rb, hanging composition and freeing E2F –> binds to DNA and stimulates transcription of genes needed for DNA replication

39
Q

What is the role of the Ras protein in cell growth and cancer?

A

proto-oncogene involved in activation of a growth factor receptor
growth factor binds to receptor –> Ras powers receptor, GTP = active, GDP = inactive
this is temporary, Ras will do this but will also reconvert back
mutation in Ras permanently turns on protein (so it’s going through this process even if there is no GTP)

40
Q

How can miRNAs and epigenetics play a role in cancer?

A
41
Q

What is the role of telomerase in cancer?

A

telomerase adds DNA back to telomeres to keep them stable after dividing
if you keep dividing, you’re going to run out of telomeres BUT mutation can cause telomerase to be permanently on (so now cells are immortal)

42
Q

Describe the steps in the progression of colon cancer

A
43
Q

oncagenes v.s. protoncagenes

A

proto: promote growth (think gas pedal in car), normally regulated
onca: inappropriately activated by mutation in cancer (pedal is stuck)

44
Q

How can a germline mutation generate Li Fraumeni syndrome?

A

inherited cell can be heterozygous (has 1 good and 1 defective TP53), if good mutates, you’re left with only bad

45
Q

How much genetic variation between humans?

A

0.1% (haploid genome ~ 3 billion base pairs)
100-200 mutations per generation

46
Q

How much effect does genetic variation have on humans? What can this be used for?

A

little to none
tracking ethnicities or migration patterns

47
Q

how do you know which SNP is the original one?

A

you don’t… if one is more predominant, that is probably the og

48
Q

retrotransposon

A

reverse transcriptase process converts RNA back to DNA, allowing genetic component to copy and paste themselves onto other parts of the genome

49
Q

DNA transposon

A

lack an RNA intermediate
encode transposase enzyme
occasionally replicate
<2% of the human genome

50
Q

OMIM allele track

A

info on mendelian disorders
phenotypic affects on mutations

51
Q

ClinVar Variants track

A

genomic positions of variants
relation between human variations and phenotypes
allows you to look at SNPs

52
Q

ENC DNA methyl track

A

regions that can be methylated

53
Q

ENC histone track

A

histone modification

54
Q

ENC TF binding track

A

transcription factor binding

55
Q

sno/miRNA track

A

where micro RNA genes are

56
Q

TS miRNA track

A

where miRNAs bind to 3’UTR of gene you’re looking at

57
Q

RepeatMasker track

A

repeat sequences (SINE, LINE, LTR)

58
Q

What is required for MPF activity and entry into mitosis?

A

cyclin b

59
Q

Activation of ___ causes degredation of cyclin b to complete mitosis

A

MPF

60
Q

steps in colon cancer

A

mutation in tumor suppressor gene (like APC)
small growth (polyp) forms on colon wall
cells dividing (but still somewhat under control), if it picks up another mutation (like ras), can divide further
continues to grow
could pick up yet another mutation (TP53)
loss of antimetastasis gene

Genetics (5 decks)

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