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Mol. Cell Bio > CH 14: Cellular Reproduction > Flashcards

CH 14: Cellular Reproduction Flashcards

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1
Q

Two major phases of the cell cycle

A

mitotic (M) and interphase

M phase is a very small portion of the cell cycle

cytokinesis is not a part of mitosis, but follows after mitosis

preceding mitosis is G2 phase

G1, S, G2, M

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2
Q

Catagories of cells

A

specialized cells that have lost their ability to divide
=> muscle cells, red blood cells

Cells that can be induced to divide
=> liver cells, lymphocytes

Mitotically active cells
=> epithelial cells, hematopoietic stem cells

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3
Q

Cell fusion experiments

A

fgusion of G1 cells with S-phase cells resulted in G1 nucleus stimulated to undergo replication

fusion of G2 cells with S-phase cells resulted in G2 nuclei not stimulated to undergo replicaiton

implicaitons =MCM protein are exported out the nucleus after replication. After replicaiton they are not present, thus not in the G2 cells and cant undergo replication

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4
Q

Mitotic factors induce chromosomal complation

A

M-phase HeLa cell fused with G1 PtK2 cells
resulted in G1 chromosome compaction. Note, M phase chromosome is HIGHLEY compacted, and G1 is not at all.
=> something in the mitotic cell to tell G1 cells to compact

fusion of Mphase Hela cell fused with Sphase PtK2 cell
=> S is very uncompacted, leads to S chromosome fragmenttation

fusion of M with G2 results in G2 compaction

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5
Q

the role of Protein kinases for cells entering M phase

A

entry into M phase initiated by protein kinases

maturation promoting factor (MPF)

MPF activting is coorelated to cyclin, that is it is DEPENDENT
=> cyclin dependent kinases

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6
Q

Discovery of MPF

A

early experiment with egg development= maturation process

progesterone stimulates first meiotic division from the primary oocyte to the ovum

“Germinal vesicle breakdown”

ratio of induced maturation to volume of injected cytoplasm is highest at 20 hours following progesteron treatment

took cytoplasm out of a fertilized frog egg (treated with projesterone) and put it into an unfertilized frog egg

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7
Q

MPF activity cycles in amphibian eggs

A

MPF activity present in cytoplasm 90 minutes after fertilization

activity correlates with cell divisions (Cleavages)

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8
Q

Cell cycle extracts from HeLa cells

A

germianl vesicle breakdown (GVBD) mazimal wtih mitotic extract

activity not present in extracts from early G1, late G1 or s phase

Mitotic extract from a somatic cell can influence egg cells to divide

thus, all cells have the same maturation promoting factor needed for that cell to ;divide

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9
Q

Protien A vs protien B iin cell division

A

protein A = cyclin. cycles up and down by increaseing right before cell division then dropping off

Protien B keeps increasing over time

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10
Q

MPF activity

A

purified MPF stimulated the incorporation of p32 into protiens and is thus a kinase

MPF consists of two polypeptides
32 kda and 45 kda
45 kda protein becomes labeled with p31 (cyclin)

Yeast produce 34 kda protein with kinase activity (cdc2)
=> antibodies from cdc2 react with amphbian 32 kda protein
=> highly conserved protein, same regualtion in all eukaryotic cells

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11
Q

Cyclin A mRNA induces maturation

A

xenopus oocytes either injected with cyclin mRNA or stimulated with cyclin mRNA or stimuated with progesterone

percentage of oocyted exhibiting germinal vesical breakdown (GVBD) measured

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12
Q

Cyclin dependent kinases

A

cdks first studied in yeast

temperature sensitive mutants idenify two stop points
=end of g1
=end of g2

fission yeast
=cdc2 responsible

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13
Q

cell cycle regulation in yeast

A

cdc2/ g1/s cyclin phosphorylated ORC

cdc2/ m cyclin phosphorylated lamin proteins

CYCLINS ARE ARE SAME but the kinases are different

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14
Q

regualtion of cdks

A

cyclin concentration
= differential transcription of cyclins at stages of cell cycle

controlled proteolysis
=cyclin concentration regulated by controlled synthesis link cyclins to polyubiquitin chain (degradation signal)

cdk phosphorylation state
=kinases CAK and Wee1
=phosphatase cdc25

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15
Q

cdk phosphorylation state

A

CAK phosphorylated Thr161

Wee1 phophorylated Tyr15
=> inactivated cdc2 kinase

cdc25 phosphatase removes Tyr15 phosphate
=> activates cdc2 kinase

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16
Q

yeast cell cycle mutants

A

wee1 mutant (kinase)= cell divides prematurely

cdc25 mutant (phosphatase)= cell continues to grow, doesn’t divide

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17
Q

Subcellular localization of cyclin

[cyclin b1]

A

G2 to prophase [m]

G2, cyclin is in cytoplasm, is then imported into the nucleus for prophase
=> phosphorylation of nuclear expport signal (NES) stops export form nucleus

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18
Q

Mammalian cyclins and cdks

A

Cyclin b/a + cdk1 initiates G2 to M phase

cyclin D’s + cdk4 cdk6 activates pRB which increases transcription of cyclins E and A

cyclin E + cdk2 initiates G1 to S phase

Cyclin A + cdk2 initates S to G2

___________________________________

cdk1 is absolutelyy required for development

mice expressing only cdk1 and cdk4 develop into sterile adults
=> defects in meiosis

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19
Q

Cell cycle checkpoints

A

delay profression of cell cycle if
=>chromosomal DNA damaged
=> DNA replicaiton not completed
=> misalignment of chromosomes

requires three classes of proteins
=> sensors that detect abnormaliates and emit signals (often kinases
=> Transmitters that send signal along pathway
=> effectors that respond to signal and inhibits cell cycle machinery

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20
Q

DNA damage checkpoints

A

G2 check
=> ATR sensor is activated by ultraciolet damage (thymadine damage) activates chk1 and then phosphrylated cdc25. cdc25 when phorphorylated in inactive

G1 check
=> ATM sensor is activatd by ionizing radiation (double stranded breaks) and activates chk2 which phosphorylated p53 and activates p21 transcription
=> p21 protein directly inhibits cdk

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21
Q

cdk inhibitor arrests cell cycle progression

A

p27 (similar to p21) alters conformation of cdk catalytic subunit

=> inhibits protein kinase activity

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22
Q

gentics of cancer [chapter 16]

A

cancers are often monoclonal
=> arise from a single cell

Malignancies require more than a single genetic alteration

inheritance of mutated genes is not the leading cause of cancer (shown in twin studies= envriomental hazzards)

Stem cells may be the source of tumors
=> natural selection for cells that have advantanges
=> i.e., telomere length

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23
Q

Genetic alterations for cancer

A

expression of telomerase

epigenetic changes
=> promoter alteration
=> methylation patterns

mutations of tumour suppressor genes
=> p53

oncogenic genes
=> growth factor receptors, and associated genes

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24
Q

tumor cell types depend on what type of tissue they arise from

A

x = tissue stem cell

y = pluripotent progenitor cell

z = commited progenitor cell

tumor cells can arise from stem cells or progenitor cells

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25
Q

Precancerous cells often exhibit histological changes

A

normal cervial epithelial cells have small nuclei and homogenous in shape

abnormal cells from cervixal carcinoma with large nuclei, heterogenous in shape (think of wee1 mutant, quick division)

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26
Q

Tumor suppressor gene // and // oncogene

A

both copies of tumour suppressor gene must be knocked out

mutationin one of two copies of oncogene sufficient (dominant)

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27
Q

Types of mutations that lead to cancer

cel cycle

A

altered protein strucutre

geneamplification - overexpression

rearrangement of DNA alters expression of strucuture

figure 16-12

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28
Q

Mutations in Rb gene lead to Cancer

A

Sporadic = individual begins with two normal alleles

Familial = individual inherits one mutated gene

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29
Q

Role of pRb in cell cycle

A

pRb bound to E2F protein
=> Trancription repressor for genes involved in G1 to S progression

Cdk phosphorylated pRb
=> Dissocated from E2F

E2F activates transcription

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30
Q

Role of p53 in cancer and the cell cycle

A

Tumor suppressor gene
=> p53 levels rise in response to DNA damage

5o % of human cacers linked to mutation in p53 gene

Activates p21 gene whose product inhibits progression form G1 to S
=> Cell repairs damage

p53 can promote cell to enter apoptocitc pathway
=> activates Bax gene

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31
Q

p53 mutations

A

frequency of mutations for p53 aminos acids

removal of positively charges Arginine whihc prevents the p53 TF from binding to the DNA backbone

most frequents mutations correleated with regions interacting with DNA

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32
Q

Role of p53

A

p53 expression increases in response to DNA damage
=> arrests cell in G1 or directs cell to the apoptotic pathway

p53 mutatuion consequences
=> mitotic failute
=> Division with damage => tumour

double p53 (-/-) mutants less susceptilble to chemical// chemothreaputic treatment. 
=> continue to divide and do not become apoptotic
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33
Q

p53 and senescence

A

Senescence
=> cells remains alive and metabolically active (non-dividing)

Senescence can be triggered by Ras oncogene (ex benign mole)

Inactivaiton of p53 leads to malignalcy
=> tumour progression

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34
Q

p53 and PST

A

posttranslational modificaitons of p53 regulate the specificity of the enzyme

phosphorylation, acethylaiton, methylation

alternateive splice variants

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35
Q

sensecence and tumorigenesis

A

cellular senescence triggered by one of two major tumour suppressor pathways, p53 and pRB

cells are blocked at the G1/ S transition

Senescent cells accumulate in aged tissues

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36
Q

Senescene associated secratory proteins (SASP)

A

have multiple effects
= inflammaiotn
= enchance proliferation of tumours

Platelet cells and tumorus interact
= tumours activate platelets
=activated platelets release factors that affect proliferation or metastasis of tumours

interactiosn of senescent cells and platelets?
= alter the functional status of platelets and fibrinolysis

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37
Q

Familial adenomatous polyposis coli (FAP)

A

inherited disorder that leads to polup formation on colon

deletion of APC gene on chromosom 5
=> one allele mutated - premalignant
=> two alleles mutated - malignant

APC = anapahse promoting complex

loss of APC functinon leads to abnormal chromosome segrefations = aneuploydy

APC gene muations = premaligants polyps in colon epithelial cells

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38
Q

Breast cancer

A

BRCA1 and BRCA2 genes linked to high proportion of breast cancers
=> respond to DNA famage and initiate repair

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39
Q

Proto-oncogenes

A

oncogenes promote loss of growth control and conversion to malignant state

approximately 100 protooncogens have been identified
=> mostly linked to processes involved in cell growth
=> often included in genomes of RNA tumour viruses

ex: sis viral oncogen derived from PDGF
: erbB encodes EGF receptor

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40
Q

Genomic landscape of colorectal cancer

A

APC and TP53 are common mutations

there are also many different unique somatic mutations

70% of colon cancers exhibit chromosome instability and aneuploidy

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41
Q

mitosis

A

process of nuclear division that faithfully partitions duplicated cvhromososmes

five stages

prophase, prometaphase, metaphase, anapahse, telophase

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42
Q

cytokinesis

A

divison of cell that partitions cytoplasm into two cellualar packages

43
Q

Prophase

A

chromosomal material condenses to form compact chromosomnes

cytockeleleton is disassembled and mitotic spindle is assembled

golgi complex and ER fragment. Nuclear envelope disperses (triggerd by phos of lamin proteins)

44
Q

Prometaphase

A

chromosomal microtubesla attach to kinetochors of chromosomes

chromosoems are moved to spindle equator

45
Q

metaphase

A

chromosomes are aligned along metaphase plate attached by chromosomal microtubules to both poles

46
Q

anaphase

A

centromeres split, and chromatids separate

chromosomes move to opposite spindle poles

spindle poles move farther apart

47
Q

telophase

A

chromosomes cluster at opposite spindle poles

chromosoems become dispersed

nuclear envelope addembles aroung chromosome clusters

golgi complex and ER reforms

Daughter cells formed by cytokinesis

48
Q

Condensin and Cohesin

A

condensin forms loop around DNA loops

Cohesin forms loop around sister chromatids
=> alternative model: cohesin forms moleucular bridges between sister chromatids

49
Q

Mitotic chromosomes

A

cohesin dissociated from sister chromatid arms during prophase
=> polo-like kinase and aurora B kinase phophorylate cohesin

remains at centromere

50
Q

Kinetochore structure

roles

A

roles:

site of attachment to mitotic spindle

location for motor proteins

components fo signaling pathway for cell cycle checkpoint

51
Q

Kinetochore structure

proteins

A

Dynein moves toward minus end of microtubule

CENP-E (kinesin) moves toward plus end of microtubule
NDC80 is a multisubunit protein that connects microtubule to kinetochore

depolymerase = specialized kinesin protein responsible for depolymerizing mt during anapahse

52
Q

Cohesin

A

dissociated from sister chromatid arms during prohpase*

remains at centromere

polo-like kinases and aurora B kinase phophorylate cohesin

phosphatase at centromere removes phosphates groups to maintain cohesin

53
Q

Roles of kinetochore structure

A

1 site of attachment to mitotic spidle

2 location for motor proteins

3 component of singaling pathway for cell cycle pathway

54
Q

kinetochore strucute

the proteins

A

Dynene = moves toward minus end of microtublules

CENP-E (kinesins) moves toward plus end of mt

deplumerases-specilized kinesin protein responsible for depolymerizing mt during anaphase

55
Q

Formation of mitotic spindle

centrosome cycle

see refrence for picture

A

phosphorylation of centrosomal protein by cdk2 initiates duplication

centroles duplicate in s phase

centrosomes migrate to opposite poles in mitotis

G1 pericentrioloar nuceation site

S duplication

G2 elongationa nd maturation

M centrosome seperation

(Holland et al 2010)

56
Q

formation of mitotic spindle

prophase

A

during prophase-spindle microtubules start to organize and emenate from centrosomes

microtubules = astral microtubules
=> these go out to the end of the cell and play an impirtant role in cytokeneisis = form the cleavage furrow

57
Q

Abnormal centrosome number

A

leads to abnormal chromosome segregation

58
Q

spindle formation in absence of centrosomes

(as in plants)

A

spindle fibres nucleated at chromosomes instead of centrosome

minus end directed motor proteins have multiple heads that cause minus ends of chromosomes to converge

multiple heads on one protein linkes and pulls microtubles together to make a spindle pole

59
Q

early prometaphase

A

immediately following nuclear envalope breakdown

chromosome become associated with plus end of microtubules

chromosomes associated randomly on a microtubule, but the motor protein activity of the motor-protein arm will direct the chromosome towards the tip of the microtubule where it will become bound

60
Q

tension

A

when a chromosome is equally lined up on the prometaphase plate, there is equal tension on either kinetochore

important signalling process

equal tension on all chromosomes means that the cell can progress towards anaphase

61
Q

role of motor proteins

A

congression of chromosomes to the metaphase plate

deficient for kinesin protein associated with the + directed chromosoems samres

chromosomes can not congress

motor protein normally provides force for moving away from arms

62
Q

microtubule behaviour

A

differential polymerization rattes regulated by differntial pulling force (tension) on chromosomes

chromosome tethered by motors (and ndc80)

tension = treadmilling
=> equal rates of polymerization and depolymerization

(figure 14-23)

63
Q

Mitotic spindle of animal cells

A

minus ends of all spindle microtubules oriented towards centrosomes

anstral microtubules = help position the spingle apparatus, may help determine plane of cytokenesis

chromosome microtubules = exert pulling force

polar microtubules = maintain mechenical integrety of spindle

64
Q

Tubulin Flux at metaphase

A

treadmilling

tubulin monomers incorperated at plus ends (kinetochores) (net gain)

monomers lost at minus ends (centrosome) (net loss)

65
Q

anaphase control

A

APC and SCF responsible for adding ubiquitin and targeting protiens to proteasomes

(APC = anaphase promoting complex)

APC^Cdc20 labels securin protein (metaphase/ anaphase)

APC^Cdh1 ubiquinates mitotic cyclins (pregresses to g1)

Cdh1 activity is inhibited by Cdk1 mediated phophorylation during mitosis. Becomes active as cdk1 activity drops

Destruction of mitotic cyclins promotes mitotis to G1 transition

Destruction of securin actvates “separase” enzyme that cleaves cohesin protiens- sister chromatids separate

66
Q

Importance of proteolysis in mitotis

A

cdk1 inhibitor added

mitotis complete, initiate cytokinesis

cdk1 is progression into mitosis.

washed free of cdk1 inhibitor, cdk1 is now active and cell goes back into mitosis becuase cyclin b was not degrated. cell thus enters mitosis again

need to degrade proteins like cyclin B to regulate teh cell cycle

67
Q

events of anaphase

A

anaphase A
=> monomers lost from plus ends of chromosomal microtubules
=> seperation of sister chromatids

anaphase B
=> monomers added to plus ends of polar microtubules
=> pushes poles apart
=> poles move apart and sister chromatids (now chromosomes) move to the poles)

polar microtubules become larger, push past each other and moves the poles furtherapart

kinetochore attachement we see
depolymerization which pulls chromosomes to the opposite ends

68
Q

micotubule depolymerization

A

catastrophic dissasembly of the microtubules causes chromosomes to move toward the basal body= organizing center

basal body-microtubule organizing center

as tubulin dimers are diluted fromsolution, microtubule ahortens and pulls chromosome toward basal body

69
Q

catastrophic disassembly of microtubules

A

chapter 9-25

GTP dimers are incorperated into tubulin

GTP to GDP dimers

in you increase the rate of hydrolysis or lower teh rate of GTP dimers, the rate of hydrolysis catches up to the rate of incorperation// polyermerisation

the flared out strucutre is more stable that linear, flared out GTP dimer structure is overtaken

=> catastrophic dissasembly

70
Q

Microtubule depolymerization (anaphase)

A

depolyermization of microtubule at both ends

depolyermizing kinesins at either end of microtubules

71
Q

Spindle (assembly) checkpoint

A

chromosome fails to attach to spindle fiber

attaches and moves polewards until stable

spindle checkpoint protein - Mad2 labeled pink
=only found on kinetochores that are mod attached to spingle fiber
= mad2 binds cdc20 not able to ubiquinate securin

mad2 blocks cdc20// degredtion process
=> no seperation

72
Q

Importance of mechanical tension

A

aurora B kinase enzyme (activity at centromere) responds to lack of tension

phophorylates unknonw substrate

destabilizes MT attachment

kinetochores reattach

73
Q

Activity of motor protein (prometaphase)

A

1 plus end directed motor proteins cause polar mictobuluels to slide past each other

2 minus end directed motor protein at kinetochore

3 plus end directed motor protein associated with kinetochore and chromosomes

74
Q

Activity of motor protein (metaphase)

A

4 plus end directed motor activity on polar microtubules

5 balanced activity of motor proteins at kinetochore

75
Q

Activity of motor protein (anaphase)

A

6 kinetochore motors move chromosomes and/or anchor chromosomes to depolymerizing microtubules

7 motor proteins separate poles

76
Q

cytokinesis

A

actin micofilaments at equator of dividing cell

=> myosin is important too

77
Q

role of myosin in cytokinesis

A

starfish egg incubated with myosin antibody whihc inhibits cytokinesis

mitotis continues in absence of cytokinesis

the two processes can be seperated

78
Q

position of spindle pole

A

cleavage plane forms between spindle poles

narrow cell divides quicker

cleavage furrow is at the midpoint between the centrosomes
=> they are responsible for formaiton// alignment of the cleavage furrow

79
Q

Position of spindle pole

A

DIntance from poles to cleavage plane is smaller in cylindrical cell

shortens time it takes the cleavage signal to reach the surface (cortexz)

equatorial stimulation

80
Q

models to explain how the mitotic apparatus signals the cortex to determine the poistion of the cleavage furrow

A

Astral relaxation
=> signals from teh astral centers induce relaxation of the cortex near the poles

Equatorial stimulation
=> by signals from the astral centers. Signals from the astral centers induce contraction of the equatorial cortex

Equatorial stimulation
=> by signals from the spindle midzone. Signals from teh spingle midzone induce contraction of the equatorial cortex

81
Q

Cytokinesis in Plant cells

A

organization of microtubule arrays changes during M phase

preprophase band-site of cleavage

phargmoplast-role in formation of cell wall\

1 folgi derived vesicles organized on cell plate

2 fingers extended that fuse with neighbouring vesicles

3 membranes fuse with original plasma membrane contents of vesicles form cell plate

82
Q

meiosis

A

mechanism to reduce chromosome number by half

two sequential cell division without an intervening rounds of DNA replication

division 1: homologous chromosoems separated

division 2: sister chromatids divide into separate chromosomes

83
Q

prophase 1 of meiosis`

A

pairinng of homologous chromosomes

84
Q

anaphase one of meiosis

A

metaphase 1 lining up of chromasomes

anaphase 1 separation of homologous chromosomes

85
Q

telophase 1 of meiosis

A

homologous chromosomes migrate to opposite poles`

86
Q

prophase 2 of meiosis

A

second meiotic division identical to mitosis

87
Q

gametic or terminal meiosis

A

all multicellular organisms

primary role is formation of gamates

88
Q

zygotic or initial meiosis

A

protists and fungi

meiotic divisions occur just after fertilizatiohn to produce haploid spores

spores mitotically divide to produce haploid adult generation

89
Q

sporic or intermediate meiosis

A

plants and some algae

meiosis not used to produce gametes

gametes produced by mitotic divisions of haploid gametophyte

90
Q

see figure

A

14-20

91
Q

meiosis and alternate life cycles

A

gametic and sporic = fusion of egg and sperm, diploid adult

zygotic = meiosis immediately after fusion of haploid spores

sporic = sporophyte meiotically divides to produce haploid spores

zytoic = spores divide mitotically to produce haploid adult generation

sporic = gametes formed from gametophyte by mitotic division

zygotic = haploid spores generated from mitotic division of adult

92
Q

meiosis in vertebrate males

A

meiosis occurs before differentiation of sperm

produces four viable gametes

spermatogonia => spermatocytes (primary) => secondery => spermatids

spermatids differnitate to become sperm

93
Q

meiosis in vertebrate females

A

meiosis occus after differentiation of the primary oocyte

produces only one fertile egg

primary oocyte arrested in prophase I until ovulation

94
Q

stages of prophase I

A

leptotene = condensed chromosomes first visible

zygotene = visivble associateion of homologues (synapsis)

pachytene = end of synapsis

diplotene = dissolution of synaptnemal complex, chiasmata visible

diakinesis = meiotic spindle visible

95
Q

end of leptotene

A

telomers organized together in a bouquet and associated with nuclear envelope

96
Q

synaptonemal complex

A

complex that holds the homologous chromosomes togeter

lateral and transverse complexs

97
Q

when does crossing over occur

A

occurs during beginning of diplotene

chiasmata are the crossing over structures

98
Q

separation of homolgous chromosomes and sister chromatids

A

sister chromatids held together by cohesins [synaptonemal complex]

homologues held together by chiasmata because after the synaptonemal complex breaking down entering metaphase I

cohesin cleaved between arms remains at centromeres

chromosomes seperate

metaphase II cohesisn breaks down and sister chromatids separate

oocyte arrested at metaphase II due to inhibitions of APC^cdc20

fertilization leaads to calcium influx and activaiton of APC^cdc20 and destruction of cyclin B

99
Q

meiotic nondisjunction

A

20-25% of human oocytes are aneuploid (monosomic or trisomic)

primary nondisjuction = incorrect segregation of homologous chromosomes
(two gamates with extra, two with none)

secondary nondisjunction = incorrect segregationo f sister chromatids
(two normal gamates, one with additional, one with nothing)

more prevelant in older egg cell because the chiasmata can let loose early and lead to early seperation of homologues

chromosome 21 trisome survies unlike many other due to gene dosage= smaller chromosome

100
Q

turner syndrome

A

XO

female with genital development arrested and ovaries fail to develop

101
Q

klinefelter syndrome

A

XXY

male with presence of feminine physical characteristics

102
Q

XYY

A

physically normal male, taller than average, supermale

103
Q

genetic recombnination

A

echange of maternal and paternal alleles during meiotic prophase I

physical breakage of DNA molecules and religation with split ends of homologous chromosomes

involves DNA repair enzymes that fill gaps furing exhange process

104
Q

genetic recombnination process

A

double strand bvreak in one chromosome

widening of gap by exonuclease activity (5’ to 3’ excision)

single strand invades homologous chromosome (Rad51 protein) and displaces strand

DNA repair using the homologous strand as a template

heteroduplex formation with a holiday junction

breakage and lreligation with resolvase enzyme to make with cross over or non-crossover products

see nexus video

Mol. Cell Bio (6 decks)

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