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Cellulaire Oncologie > SP-HC4: Alberts h17 (Cell Cycle) > Flashcards

SP-HC4: Alberts h17 (Cell Cycle) Flashcards

1
Q

The cell cycle checkpoints

A

-Metaphase to anaphase: are all chromosomes attached to spindle? proceed to cytokinesis
-G1/S checkpoint: is the environment favorable? proceed to S-phase
-G2/M checkpoint: is the DNA replicated and is the environment favorable? proceed to mitosis

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2
Q

The cell cycle is regulated by cyclins. Name the types of cyclins.

A

-G1/S cyclins: activate Cdks in late G1
-S cyclins: start/help DNA duplication
-M cyclins: stimulate entry into mitosis

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3
Q

To which enzymes do cyclins bind?

A

Cyclin-dependent kinases (Cdks) > checkpoint molecules

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4
Q

Which cyclins are active in which cell cycle phases?

A

G1/S cyclin: during G1 phase
S-cyclin: during late G1, S, G2 and M until metaphase-anaphase
M-cyclin: during late G2 phase until metaphase-anaphase

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5
Q

How are Cdks activated?

A

A cyclin binds to a Cdk > the T-loop will expose and a CAK (Cdk-activating kinase) will phosphorylate the loop for activation

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6
Q

Wee1-kinase

A

A kinase which can add an additional phosphate group to an active Cdk-cyclin complex, which inactivates the complex (inhibitory phosphate)

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7
Q

Cdc25 phosphatase

A

Cdc25 can remove the additional inhibitory phosphate on a Cdk-cyclin complex > reactivation

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8
Q

p27

A

p27 can bind an active Cdk complex which inactivates it > safety mechanism (like a clamp on the complex)
> p27 is mutated in cancer cells > proliferation
> p27 regulation through gene expression

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9
Q

Positive feedback mechanism of M-Cdk

A

PP2A-B55 phosphatase dephosphorylates Cdk-substrates for inactivation/
- Active M-Cdk activates Greatwall kinase
> Greatwall kinase activates Ensa
> Ensa inactivates PP2A-B55
- M-Cdk activated Cdc25 by phosphorylation and removes inhibitory phosphates from M-Cdk molecules

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10
Q

PP2A-B55 inhibitory mechanisms

A

-Dephosphorylate Cdk-targets
-Inactivate Greatwall kinase
-Dephosphorylation Wee1 > activation (inhibitory phosphate)
> Wee1 adds inhibitory phosphate to M-Cdk

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11
Q

M-Cdk main function

A

Phosphorylate substrates which lead to mitosis

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12
Q

Function APC/C

A

Anaphase-promoting complex or cyclosome > ubiquitin ligase > initiation proteolysis in proteasome

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13
Q

Targets APC/C

A

-Securin: securin inhibits separase, the sister chromatid seperator enzyme
-S- & M-cyclins: Cdk inactivation by breakdown of cyclins

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14
Q

APC/C pathway with Cdc20 / Cdh1

A

In M-phase
-M-Cdk phosphorylates APC/C and Cdh1
-APC/C binds Cdc20 > activation
-APC/C-Cdc20 initiates anaphase and inactivaties M-Cdk by ubiquitination of M-cyclin
-APC/C is dephosphorylated and inactive (unbinding of Cdc20 due to conformation)
-Cdh1(P) is inactive
Onset G1-phase
-M-Cdk inactivation by APC/C leads to dephosphorylation of Cdh1 > activation
-Dephosphorylated APC/C can bind active Cdh1 > activation
-APC/C-Cdh1 keeps destructing M-cyclin and thereby inhibiting M-Cdk

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15
Q

DNA damage can influence checkpoints. How?

A

Inhibit G1/S-Cdk, S-Cdk, M-Cdk
> S-Cdk and M-Cdk prevent DNA re-replication

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16
Q

How is one time replication regulated?

A

Assembly of PreRCs (block the replication origins) > inhibited by Cdks and activated by APC/C
>Low PreRCs during S-phase and G2-phase

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17
Q

S-Cdk DNA replication pathway

A

Prevention new duplication: phosphorylation of Orc (origin recognition complex) during S/G2/M
- S-Cdk activation stimulates assembly of Cdc45 and GINS at each Mcm helicase (inactive)
-DDK (a kinase) phosphorylates Mcm helicase forming an active CMG helicase (complex of Cdc45-Mcm-GINS) > unwinding DNA > trigger DNA-polymerase activity

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18
Q

Prophase

A

Condensation of sister chromatids which are still closely associated. Assembly mitotic spindle between 2 centrosomes.

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19
Q

Prometaphase

A

Breakdown nuclear envelope > microtubuli can reach the chromatids. And further condensation of sister chromatids

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20
Q

Metaphase

A

Chromosomes are localised in the equatorial axis and the kinetochore MTs bind the sister chromatids at opposite poles of the spindle

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21
Q

Anaphase

A

Sister chromatids seperate in sinc because of shrinkage of kinetochore MTs.
Spindle poles move apart from each other due to elongation of the spindle

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22
Q

Telophase

A

Sets of daughter chromosomes arrive at the poles and decondensate, a new nuclear envelope is made around the set of chromosomes and the contractile ring starts forming.

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23
Q

What characteristic means the end of mitosis

A

Forming of 2 new nuclei

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24
Q

Cytokinesis

A

Division of the cytoplasm by the contractile ring consisting of actine and myosine

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25
Q

Centrosome division

A

Early in cell cycle
-G1: procentriole site selection
-S: centriole duplication
-Entry into M-phase:
> Removal tether between centrosomes
> centriole and centrosome maturation
> centrosome seperation
-Licensing (start G1)
> contriole disengagement and centriole-to-centrosome conversion

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26
Q

Where are the kinetochores located most of the times?

A

At the centromeres

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27
Q

How many winds of DNA around a nucleosome core particle?

A

2.5x

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28
Q

Cohesins

A

Cohesins hold the sister chromatids toghether tightly
> Smc molecules with ATPase domain > dimer binds ATP
>Scc molecules as a clamp around Smc-heterodimer
>Smc dimer forms a loop around the sister chromatids

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29
Q

Condensin

A

Can get the DNA into a more spiral conformation> more condense

30
Q

Where are cohesins located?

A

At the places where the sister chromatids make contact

31
Q

Three classes of microtubules form the mitotic spindle. Name them

A

-Kinetochore MTs: connect to the chromosomes
-Interpolar MTs: making bipolar connection with each other in the spindle (plus and minus ends connection)
-Astral MTs: polar MTs radiating outside

32
Q

Kracht maken van microtubules

A

Multimere motoreiwitten induceren minus-end foci > kracht via sliding antiparallel microtubules

33
Q

Krachten via kinesines

A

Lopen naar plus-end
> Kinesin-5 loopt met 2 uiteinden naar plus end > antiparallele crosslinking (door op 2 MTs naar plus te lopen zorgen ze voor wegduwen van minus ends van interpolar MTs)
>Kinesin-14 heeft 1 stabiele binding site en 1 motor domein van 2 heads, beweegt naar plus-end (zorgt voor push door binden een MT van ene pole en dan op MT van andere pole naar plus lopen waardoor plus van de motor domain push)
> Kinesin-4/10 > outward push van zusterchromatiden (bind zusterchromatide die al wordt getrokken en loopt naar plus end voor duwen microtubule naar het midden toe voor push)

34
Q

Krachten van dyneines

A

Lopen naar minus end > tegenkracht (houden de cell cortex vast en door lopen naar minus-end een kracht naar de plus end en ruimte maken)

35
Q

Ran-GTP is vooral actief rond de chromosomen, noem de functie en reden tot lokalisatie

A

Functie: stimulatie microtubule nucleatie en stabilisatie
- Ran-GEF is geassocieerd met de chromosomen
-Gradiënt richting periferie door delay tot hydrolyse tot Ran-GDP

36
Q

Ran-GTP en spindle formation

A

Met Ran-GTP wordt er bias aangelegd voor MT nucleatie rond de chromosomen, voor de rest is vorming spindle random proces. > spindle formatie door zelforganisatie met motoreiwitten.

37
Q

Search-and-capture mechanism

A

De kans van kinetochore-MTs om tegen een kinetochore te botsen is een kansproces via dynamische instabiliteit > kinetochore de stabiliserende structuur.

38
Q

Kinetochore opbouw

A

Inner kinetochore: centromeric nucleosome
Outer kinetochroe: Ndc80 complex die MTs stabiliseren (filamenten die MT attachment sites vormen)

39
Q

Oriëntatie kinetochoren bij metafase

A

Bi-oriëntatie van de zusterchromatiden, kinetochoren naar aparte centrosoom polen

40
Q

Hoe ontstaat de bi-oriëntatie van zusterchromatiden (tijdens mid prometafase)

A

Trial-and-error: tension sensing door Aurora-B kinase > missen tension geeft inhibitoir signaal: loslaten fosforylatie Ndc80)
> stabiel wanneer er tension van de kinetochoren vanuit beide kanten is.
>Bi-oriëntatie

41
Q

Te weinig trekking gedetecteert door Aurora-B pathway

A

Te weinig tension
> Aurora-B kinase fosforyleert Ndc80 complexes
> Inhibitie microtubule attachment
> Tension laat Aurora-B uitgaan

42
Q

Dynamiek van mitotic spindle

A

-Continue groei bij plus-end
-Continue krimp bij minus-end
-Sliding movements bij overlappende MTs
-Treadmilling

43
Q

Chromosoombeweging tijdens anafase (2 mechanismen)

A

-Kinetochore MT krimp (pull)
-Astral ejection force: interpolar of astral MTs met plus-end directed kinesin-4/10 (sliding force/afstoting richting minus-end door groei aan plus-end) zorgt voor duwbeweging centrosomen van elkaar af (push) (> eerst trekken centrosomen naar de periferie door vasthouden aan cell cortex, dan duwbeweging)

44
Q

Anafase 1 en Anafase 2

A

Anafase 1: kinetochore pulling
Anafase 2: interpolar/astral sliding pushing force

45
Q

APC/C-Cdc20 stimulatie van anafase

A

Checkpoint voor de anafase: wanneer de chromosomen verbonden zijn aan de kinetochoren dan zorgt Cdk-M via APC/C voor relief van inhibitory signal
> APC/C zorgt voor ubiquitilation en degradatie van securin die als inhibitor van seperase werkt
> Separase maakt cohesines kapot > scheiding zusterchromatiden

46
Q

Snelheid chromosoom segragatie

A

Snelheid segregatie is gelijk aan flux snelheid van de microtubuli = constant (niet versnellend)

47
Q

Stadia van cytokinese

A

Initiatie
> Contractie actine en myosine filament in contracile ring
> Membraan insertie
> Completie

48
Q

Waaruit bestaat de contractile ring en waardoor wordt de vorming gestimuleerd?

A

Actine en myosine-II
> Stimulatie door RhoA

49
Q

Completie van de cytokinese

A

Vorming mid-body, gemaakt uit de overlap van MTs en actine.

50
Q

Actieve RhoA functies

A

-Activatie formine: actine filament formatie
-Activatie Rho-associated kinases incl ROCK> myosin-II activatie
-Totale assembly en contractie van actine-myosine contractile ring

51
Q

Welke kinase uit de anafase kan RhoA-GEF activeren?

A

Aurora-B kinase

52
Q

Modellen voor positioneren contractile ring

A

-Astral stimulation model
-Central spindle stimulation model
-Astral relaxation model

53
Q

Hoe wordt het vlak van cytokinese bepaald bij dierlijke cellen?

A

Door de microtubules van de mitotic spindle tussen de polen in

54
Q

Verschil metafase plaat bij mitose en meiose-I

A

Mitose: homologe chromosomen liggen los van elkaar
Meiose-I: homologe chromosomen zijn gepaard > segregatie maternale en paternale chromosmen at random

55
Q

Welk genetisch diversiteits mechanisme kan opspelen bij meiose-I?

A

Crossing-over

56
Q

Vind er na meiose-I en voor de meiose-II nog nieuwe DNA replicatie plaats?

A

Nee

57
Q

Meiose-II scheiding

A

Segragatie zusterchromatiden per 1 van de 2 homologe chromosomen

58
Q

Hybride chromosomen kunnen bij meiose ontstaan indien….

A

crossing-over

59
Q

Hoe worden homologe chromosomen gepaard?

A

Via transverse filaments van het synaptonemale complex

60
Q

Synapsis

A

Alignment van homologe chromosomen > synaptenemal complex

61
Q

5 phases of synapsis

A

-Leptotene; seperated homologous chromosomes
-Zygotene: assembly synaptonemal complex
-Pachytene: assembled synaptonemal complex
-Diplotene: disassembling synaptonemal complex
-Diakinesis: seperated homologous chromosomes

62
Q

Mitogens can stimulate the activity of these Cdks

A

G1-Cdk and G1/S-Cdk

63
Q

Name Cdk activating mitogens

A

PDGF, EG

64
Q

Mitogen pathway

A

Mitogen (PDGF/EG) binds receptor
> Ras / MAPK route
> Expression of Myc
> Myc upregulates G1-cyclins (D-cyclins)
> Activation G1-Cdk
> G1-Cdk inactivates Rb protein (an inhibitor of E2F)
> Active E2F stimulates expression of G1/S cyclin (E-cyclin) and S-cyclin (A-cyclin)
> Activation S-Cdk > DNA synthesis

65
Q

Loss of both Rb alleles leads to

A

Retinoblastoma (inherited eye cancer)

66
Q

p21 tumor suppressor pathway

A

DNA damage
> Phosphorylation p53 due to certain kinase activations
> Mdm2 (inhibitor of p53) released from p53
> p53 binds regulatory region of the p21 gene
> expression p21
> p21 inhibits G1/S-Cdk and S-Cdk by binding their Cdk-cyclin complexes as a clamp

67
Q

Excessive Myc production and p21-route

A

Excessive Myc
> Synthesis Arf
> Arf binds Mdm2 > inactivation Mdm2
> p53 stable and active
> Expression p21
> cell cycle arrest or apoptosis

68
Q

Function of active Mdm2

A

Degradation of p53

69
Q

mTORC1 complex

A

Is regulated by growth factor receptor (enzyme coupled) cascade or by incoming diffusing amino acids (factors for cell growth and proliferation)
> mTORC1 complex regulates protein synthesis, lipid synthesis, protein turnover

70
Q

Cel proliferatie gaat gepaard met …

A

Celgroei (celgroei gemedieerd door mTORC1 complex)

Cellulaire Oncologie (14 decks)

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