Lecture 16 Flashcards
events in cell division
cell cycle :
growth
chromosome duplication
chromosome segregation
cell division
4 stages of the cell cycle
G1 = gap, cell grows
S= synth of DNA (DNA rep)
G2 =gap, preparing for mitosis
M = division ( nucleur division dn seg of chromosomes)
G1, S and g2 =period bn 2 M phases = interphase
G1 = crucial decision making stage
is the growth stage
makes sure no DNA damage, enough macromolecules, encough organelle, in favourable enc nad that there is signal to proceed (mitogens, ex. some growth factors)
everything good = go to S phase
conditions are not met = stay in G1 until fixed
if cell doesn’t need to divide (muscle or nerve cells) go to G0 phase, can re enter
terminal diff = can’t re enter.
divide, wait, rest, or die
S phase
DNA rep stage
duplicating DNA molecules
G2 phase
duplication of centrosome
reorg of microtubules
M phase = cell division stage
nucleur division dn cytoplasmic division
5 stages
prophase
prometaphase
metaphase
anaphase
telophase
prophase
duplicated chromosomes condense
nuclear envelope still there
2 centrosome duplicated and close to each other,
convert inter-basic chromosomes to mitotic chromosomes, done using protein called condensin
mitotic spindles assemble bn 2 centrosomes
centrosomes move apart
microtubeles growing from centrosomes, some towads middle some growing towards plasma mb, imp in seregation of chromomses
Imp to from before the nucelar envelope is destoryed. To make a framework to catch the chromomes
Microtubules that grow towards e/o, meet eachother. int w proteins that bind to both of them
Interpolar microtubules = being stabilied by proteins that bind them
Binding = framework being created
prometaphase
Nuclear envelope breaks down
Mitotic spindles catch chromosomes at centromeres
Lamin proteins under envelope get phosphorylated = nuclear envelope breaks down to vesicles (bc mesh work is affected) = envelope is fragmented and binds itself to vesicles
Chromosomes are released and att to mitotic spindle fibres . Via centromere
Each sister chromatid has its own centromoere and each has a complex called kinetoccohore assemebles, the microtubules bind to this
The + end always polymerizzzed nad depolyerixed
metaphase
Microtubule bring chromosomes in middle of cell, will have tubules bind kinetchore
Have interpolar microtubule (allow formation of mitotic spindles)
Aster microtubule (ones thay grow towards plasma mb ,outwardly)
Anaphase
2 sisters, once att, cohesions are now degraded, free to move to opp poles ( bc tubules assoc w sisters are shrinking/getting shorter, pulling twos opp poles)
The interpolar microtubule assoc to e/o through int w motor proteins,kynesisn start walking towards + end of microtubule so slides the microtubules further from each other. What also helps in segregation from chromosome
In cell cortex, aster microtubules in contact w plasma mb(cell cortex). Here motor porteins int w cell cortex, and walk toward - end of the microtubule (at centrosomes) bring/drag centrosome towards plasma mb
Diff forces cont to seg of sister chromatids. (3 factors overall I think)
Telophase
Chromosomes are far apart.
Nuclear envelope is reformed, lamina proteins are dephosphorylated and re interact w eachtoher to reform the envelope. Create meshwork of protiens
Int w chromosomes = ensures nuclear envelope surr chromosomes again
Envelope and pores are formed and proteins assoc w nucleus come back again
division of cytoplasm begins
cytokinesis
cytoplasm divided In 2 by a contract ring of actin and myosin filaments
Uses structures left behind by motisis
Interpolar microtubules bind other protiens that signal cell cortex to assembles actin and myosin to create contractile rings which bring the 2 sides of the cell together, creates the cleavage.
cell cycle control system , what it is, what it do, when
tiggers the major porcess of the cell cycle
makes sure events happen in correct order
can temporarily stop at transition points
- G1 to S
- G2 to M
- metaphase to anaphase.
what does it actually depend on
depends on cyclin-dependent protein kinase
Cdk’s
must bind to cyclin to become active
cyclin/Cdk complex phos. proteins involved in progression of cell cycle
different types of cyclin and cdk’S
specific pairing tells it which protein to modify - helps reco its target.
diff types of cdks
G1 CDK = resp for beginning of G1
G1/S CDK = resp for transition. here is active, where cyclin is present.
S CDK = present in S phase and G2
M CDK = starts being active at end of G2 or beginning of mitosis and then activity drops = allows cell to exit mitosis and finish w cell division
activity of cdk can be regulated
by cylin degradation, (phos and dephos = active/stopeed)
if need time for repair damage, for ex.
or by binding to a Cdk inh.
what triggers cell division up to DNA rep
mitogen = growth factor binds to a receptor, triggers a signalling pathway
Goal is to activate G1 CDK, once CDK is active it will target an inh of e2f = an imp transcription factor.
Active G1CDK phos a portein called Rb, which usually ing E2F form working, now that Rb is phos, it lets go of E2F, E2F becomes active, turns on genes needed for DNA rep. Now cell moves to S phase.
initiation of DNA rep
S CDK is needed, tells cell to start DNA rep.
phos. helices at replication origin, other proteins join in and DNA rep starts.
- makes sure DNA rep only happens once, so degrade proteins needed fro recruitment of helices
now we phos. Cdc 6 to prevent from re initiating dna rep after alr started .
DNA damage
will pause the cell cycle if DNA damage occurs.
if cell sees damage, protein kinase gets activated
that protein phos. p53 = stabilizing it + activated
when stable/active, binds to p21 gene, transcribed, translated.
p21 = a CDK inh, binds to G1/S CDK and S CDK to inactivate them
allows for time for repair or triggers cell death ia
anaphase, metaphase monitoring for error in transition state
in pro metaphase, chromosomes are lined up at equator, and each sister chromates needs to be att to one centrosome.
normally, APC (anaphase promoting compelx) tags cyclins, degrades them so conc of M CDK dec = exit mitosis
if problem, if only 1/2 sister chromatids are att = lack of tention = APC is inh
with an inactive APC, M CDK levels stay the same, so cell stays in metaphase longer to make sure both chromatids are att to the centromeres at opp poles.
eventually, will connect right = tension = inh on APC is removed = tags cyclins = cyclins degraded = m CDK is inactive = cell can exit mitosis
