biology 302 exam 4

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what is the “genetic” approach to studying a biological problem?

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1

what is the “genetic” approach to studying a biological problem?

look for mutants in which the process is defective

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2

what is spontaneous?

uncorrected errors in DNA replication and natural mutagens (xrays, gamma rays, UV light)

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3

what is induced?

expose population to mutagen

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4

what is the genetic approach to understand a process?

  1. do mutagenesis

    1. perform a mutant “screen”

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5

what is mutagenesis?

expose a population to mutagen

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6

what is mutant screen?

look for mutants that have a phenotype affecting the process of interest

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7

what did beadle and tatum do?

a genetic screen for neurospora mutants which had defects in biochemical pathways for making vitamins and amino acids

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8

what is the plan of beadle and tatum’s experiment?

isolate auxotrophic mutants which can’t make specific vitamins or amino acids

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9

what happens if you expose the haploid spores to a mutagen?

it introduces random mutations in the genes

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10

where can wild type e.coli grow?

on plates containing only lactose

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11

what are lac- mutants?

auxotrophic mutants that were unable to grow with lactose as an energy source

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12

what are lacc mutants?

mutants that expressed the lac operon genes constitutively, even in the absence of lactose

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13

what are lacl^s mutants? (superrepressor)

mutants that never expressed the lac operon genes, even in the presence of lactose

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14

what is the 1st step of genetics to study a biological process?

genetic method in the single cell eukaryote yeast to understand regulation of the cell cycle

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15

what is the 2nd step of genetics to study a biological process?

genetic method in the plant to understand control of flower development

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16

what is the 3rd step of genetics to study a biological process?

genetic method in the nematode roundworm to understand control of cell fate specification during animal development

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17

why do geneticists use brewer’s yeast to study basic processes that occur in eukaryotes?

  • single celled

  • basic cellular processes are the same as more complex, multicellular animals

  • fewer genes than in multicellular

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18

what happens during a mitotic cell cycle?

1 cell divides into 2 → mother cell budding off a new daughter cell

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19

what did hartwell do to study the eukaryotic cell cycle?

mutagenized yeast, then screened temp-sensitive mutants that couldn’t complete the cycle

  • grow the mutagenized cells at 23°

  • make a copy of the plate

  • shift 1 copy to 36°

  • look for colony that grows on 23°; not 36°

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20

what was the end product of hartwell’s experiment?

dozens of temp-sensitive mutant strains w/ a mutation in each strain

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21

what did hartwell call the temp-sensitive mutant strains?

cdc genes = cell division cycle mutant

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22

what was the conclusion of hartwell’s experiment?

the mutated gene makes a protein required to proceed thru that specific step in the cell cycle

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23

what did they find out about cdc genes?

conserved in eukaryotes, and controlled the cell cycle in other species

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24

what are homologous genes/homologs?

a gene present in 2 species b/c of descent from a common ancestor

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25

what is the ‘model system’ approach?

taking the genetic approach to study a process in a simpler species can yield results relevant to other species

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26

why does the model system approach work?

because genes are conserved and perform the same/similar functions in different species

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27

where do stem and branches grow from?

shoot meristem

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28

where do roots grow from?

root meristem

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29

where do flowers grow from?

inflorescence (flower) meristem

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30

how is the flower in Arabidopsis thaliana organized?

4 whorls

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31

what is whorl 1?

sepal

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32

what is whorl 2?

petal

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33

what is whorl 3?

stamen = makes male gametes (pollen)

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34

what is whorl 4?

carpel = makes female gametes (ovule)

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35

what did elliot meyerowitz at the caltech lab do?

mutant screen and identified mutants in which flowers developed incorrectly

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36

what did elliot meyerowitz screen in the Arabidopsis thaliana flower experiment?

mutants in which the wild type flower structure was not made

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37

what are the 3 classes of the Arabidopsis thaliana flower mutants?

  1. no sepals/petals

  2. no petals/stamens

  3. no stamens/carpels

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38

what does the wild type of the Arabidopsis thaliana flower look like?

knowt flashcard image
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39

what did elliot meyerowitz hypothesize?

whorl identity is controlled by the combination of genes expressed in that whorl

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40

what does whorl 1 do?

has class A genes - tells cells to form sepal

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41

what does whorl 2 do?

has A + B genes - tells cells to form petal

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42

what does whorl 3 do?

has B + C genes - tells cells to become stamen

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43

what does whorl 4 do?

has C genes - tells cells to become carpel

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44

whorl identity model

knowt flashcard image
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45

when the genes are identified, what did the transcription factors encode in the flower experiment?

express where the model predicted, combine with each other in pairs, regress each other’s expression, regulate downstream targets to specify organ made

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46

where do all complex, multicellular organisms develop from?

a single cell; fertilized egg

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47

what is undifferentiated?

has not adopted a distinct cell fate

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48

what are cell intrinsic factors?

traits that are “intrinsic” to a person rather than being determined by that person's environment

<p>traits that are “intrinsic” to a person rather than being determined by that person&apos;s environment</p>
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49

what is extracellular signaling?

cues designed to transmit specific information to target cells

<p></p><p>cues designed to transmit specific information to target cells</p>
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50

what are the vulva precursor cells (VPCs)?

cells in the skin of the animal (hypodermis)

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51

where do VPCs sit?

underneath the anchor cell (AC) → cell in the gonad

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52

are the VPCs born knowing their fate or are they instructed?

VPCs born not knowing what fate to adopt, anchor cell must tell them to adopt the 1° and 2° fates

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53

what causes cells to adopt the vulva fates?

activation of the RAS pathway

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54

what is cancer?

uncontrolled and inappropriate growth of cells

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55

what is a benign tumor?

tumor that remains in the spot where it grew; usually not dangerous unless it presses on other organs

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56

what is a malignant tumor?

a tumor that can invade surrounding tissue and spread

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57

what is a metastatic tumor?

a second tumor caused when cells from the primary tumor move thru the body to colonize a new site

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58

what is cancer a group of?

disorders characterized by the overgrowth of cells in different organs/tissues of the body

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59

what are some common properties of cancer cells?

  • evading apoptosis

  • self-sufficiency in growth signals

  • insensitivity to anti-growth signals

  • sustained angiogenesis

  • tissue invasion and metastasis

  • limitless replicative potential

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60

how do cancer cells divide?

uncontrollably

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61

what are growth factors?

proteins secreted by cells that cause other cells to divide by ‘pushing’ them into the cell cycle

  • bind receptors on the cell surface

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62

what happens when the growth factors bind?

it activates signaling pathways that turn on expression of genes that instruct the cell to move thru the cell cycle and divide

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63

do cells need growth factors?

no

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64

what is apoptosis?

a damaged cell commits suicide by an orderly destruction of the cell (without causing an inflammatory response)

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65

what do cancer cells display?

transformed phenotype in tissues

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66

what is angiogenesis?

formation of blood vessels

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67

what is tumor angiogenesis?

cancer cells can recruit blood vessels to themselves, allowing a tumor to grow beyond a certain small size

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68

what happens if cancer cells move away from their site of origin?

they enter the bloodstream and move to a new site in the body

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69

what type of disease is cancer in humans?

genetic

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70

what percent of the time is the cancer sporadic?

90%w

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71

what percent of the time is the cancer hereditary?

10%

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72

what is clonal?

all cells in the tumor are progeny of 1 cell

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73

what is the ‘multi-hit model’ for carcinogenesis?

cells becoming cancerous is a rare event that only happens after a number of key genes have been mutated in the same cell

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74

what are oncogenes?

genes in which gain-of-function mutations contribute to cancer

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75

what manner do oncogenes act in?

dominant

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76

how many mutated copies does oncogenes need?

one

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77

what are proto-oncogenes?

normal genes

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78

what is Ras/GTPase?

protein found on the inside of the plasma membrane

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79

what is the function of Ras/GTPase?

acts as a switch

  • GDP bound, it is off

    • GTP bound, it is on

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80

what are tumor suppressor genes?

genes in which loss-of-function mutations contribute to cancer in a recessive manner

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81

what is the cell cycle checkpoint?

a point in the cell cycle in which the state of the DNA or chromosomes is checked, and if it is not correct, then the transition to the next stage doesn’t happen

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82

where is damaged DNA checked for?

  • G1/S

  • S phase

    • G2/M

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83

what is p53?

a transcription factor protein that turns on the expression of many genes

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84

what is the Mdm2 protein?

it exports p53 from the nucleus into the cytoplasm, where it is destroyed

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85

what happens when damaged dna is detected?

p53 senses the damaged dna, p53 is not destroyed and moves into the nucleus to turn on genes:

  • genes that cause the cell cycle to arrest

  • genes that encode dna repair enzymes

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86

what does p53 turn on if damage is really bad?

genes that cause apoptosis

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87

what happens with a loss of p53?

eliminates the dna damage cell cycle checkpoints

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88

what kind of mutations are in the BRCA1 and BRCA2?

germline mutations

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89

what does mutations in BRCA1 and BRCA2 predispose a person to?

breast and ovarian cancer

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90

what are the percentages for breast cancer?

  • 12% of women will develop breast cancer at some time in their lives

  • 60% of women who inherit the BRCA1 mutation will, by age 70

  • 55% of women who inherit the BRCA2 mutation will, by age 70

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91

what are the percentages for overian cancer?

  • 1% of women will develop ovarian cancer at some time in their lives

  • 60% of women who inherit the BRCA1 mutation will, by age 70

  • 15% of women who inherit the BRCA2 mutation will, by age 70

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92

what is the hayflick limit?

normal cells, when placed in tissue culture, can divide their dna about 50 times

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93

what is replicative senescence?

normal cells are unable to divide after the hayflick limit

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94

why does replicative senescence occur?

there is no expression of telomerase gene in most differentiated cells, and telomere ends degrade

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95

how do cancer cells bypass replicate senescence?

they turn expression of telomerase back on = immortal

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96

what is biotechnology?

the field of applied biology in which living organisms, or processes from living organisms, are used, usually w/ human modification, to serve some some scientific or medical purpose

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97

genetic engineering

methods that rely heavily on knowledge from basic research into the genetics and molecular biology of model organisms

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98

what is a genetically-modified organism?

an organism which has had its genome modified in some way by human intervention

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99

what is the first reason for GMOs?

to make large quantities of a protein or drug in bacteria, animals, or plants

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100

what is humulin?

human insulin made in bacteria

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