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cell cycle, quiescence, senescence, terminal differentiation and apoptosis…
cell cycle, quiescence, senescence, terminal differentiation and apoptosis in animal cells
the cell cycle
controlled by cyclin
regulated by Cyclin dependent kinases (CDks)
active site of CDk links with cyclin with the T loop --> cyclin is partly active
once the T loop is phosphorylated --> cyclin is fully active
levels of cyclin throughout the cell cycle
late G1
rising G1/S cyclin levels lead to the formation of G1/S-CDk complexes that trigger progression through the start transition
S phase
S-CDk complexes form at the start of S phase and trigger DNA replication as well as some mitotic events
G2 phase
M-CDk form but remain inactive
activated at the end of G2 --> trigger entry into mitosis at the G2/M transition
separate regulatory protein complex (APC/C) initiates the metaphase to anaphase transition
cell states
quiescence
actively maintained state
signalling pathways are involved in maintaining a poised state
rapid activation
= G0 phase
separate phase between G1 and S phase
in absence of proliferation signals
in presence of negative regulators the cell is said
cells in G0 can re-enter the cell cycle
adult liver cells re-enter the cell cycle for tissue maintenance or repair
how can cells leave quiescence
growth factors
cytokines
hormones
chemical agents
mitogens
average rate of cell division varies with cell type (= with time spent in G0 phase)
once past G1 phase cells will complete cell cycle within 12 hours
gut stem cell
mean division rate
once every few days
state
cycling
adult liver cell
mean division rate
1 year
state
resting
peripheral neuron
mean division rate
never
state
terminally differentiated
terminal differentiation
permanent withdrawal from cell cycle
also into G0 phase
irreversible loss of possiblity of proliferating
loss occurs while acquiring specialised functions
examples
keratinocytes in skin
goblet secretory cells
enterocytes (absorptive) cells
gut epithelial cells
Senescence
cell no longer capable of dividing
there is a limit to the number of times cells can divide
stem cells are an exception
still alive
metabolically active
contributing factors
telomere erosion often ultimately triggers replicative senescence
telomeres = hundreds of repeats of the same sequence to avoid shortening of coding genes
accumulation of proteins which inhibit CdK
cancer cells evade senescence
immortality
after 60-80 rounds of division --> shortened telomeres --> damage response --> sensecence
senescence can be overcome by
activating telomerase
mutations in cell cycle protein
apoptosis = programmed cell death
normal phenomenon
genetically regulated process
leads to death of cell
controlling cell number in multicellular animals
cell number is a balance between cell proliferation and apoptosis
aim = removal of unwanted cells in an organised way
webbing between digits during animal development
excess neurons
cell death matches number of neurons to number of target cells