cell division morphological changes in m-phase due to protein phosphorylation, dephosphorylation...
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Cell Division
Morphological changes in M-phase
due to protein phosphorylation, dephosphorylation
• Chromosome condensation: histone
• NEBD: nuclear lamins
• Cytoskeletal rearrangement(spindle, contractile ring): caldesmon, c-src
Centrosome cycle
• Formation of mitotic spindle pole• Independent to nuclear cell cycle• S-phase: centriol replicate• Prophase: centrosome split & move apart• Prometaphase:
NEBDmt from each controsome to enter nucleus, &interact with chromosome spindle pole
Prophase
• Chromosome condensation: form 2 sister chromatids held together at centromere
• Centrosome split & move apart• Dynamic microtubules: Half life of MT decreased 20X
Prometaphase
• Centrosome segregate to the pole
• NEBD at early prometaphase– Enables mitotic spindle to interact with chromosome
• Formation of mitotic spindle
– Kinetochore MT: orientation and movement of chromosomes– Kinetochore act as cap that protect + end from depolymerizing– Centrosome at spindle pole protect – end from depolymerizing
Formation of bipolar mitotic spindle
MAP (motors) stabilizes
Dynamically unstable + end
+ end overlap
Kinetochore
• Developed from centromere
• MT attaches in metaphase
• Consist of a specific DNA sequence
• Large mutiprotein complex, platelike trilaminar structure
• Human; 20-40 MT, yease; 1 MT
• A puzzle: how MT & kinetochore connected to each other * hold on to a MT end, yet allow that end to add or loose subunits
Aster exclusion force
• The origin is not known• Aligning chromosomes at the spindle
Evidence for an astral ejection force
How MT & kinetochore connected to each other
• Microinjection of labeled tubulin:
• metaphase; incorporate tubulin near kinetochore• anaphase; reverse action at same site
• Puzzle:
• Hold on to a MT end, yet allow that end to add or loose subunits
• Sliding collar based model
• Microinjection of labeled tubulin:- metaphase; incorporate tubulin near kinetochore- anaphase; reverse action at same site
Anaphase• Paired kinetochore separate –> separation & segregation of chromatid• Start abruptly by specific signal• Signal may be intracellular Ca2+ rise: 1) Rapid, transient 10X increase Ca2+ at anaphase in some cells 2) Injection of low level of Ca2+ into metaphase cell ->premature anaphase 3) Accumulation of Ca2+ containing membrane vesicle at spindle pole 4) Clamp Ca rise by EGTA, BAPTA -> arrest anaphase
**mechanism of Ca2+ rise during anaphase is a mystery
• Anaphase A shortening of kinetochore MT -> poleward movement of chromatids no energy required for shrinking of kinetochore
• Anaphase B elongation of polar MT -> two spindle poles move further apart ATP hydrolysis is required for elongation of polar MT; kinesin ATPase drug chloral hydrate inhibits Anaphase B not A
pulling aster MT -> -end moter binds cell cortex & aster MT-> pull spindle pole apart
Telophase
• Chromatids separate completely
• Kinetochore MT disappears
• Polar MT elongate still more
• Nuclear envelope reassemble
• Nucleoli reappear
Cytokinesis
• Begins at anaphase
• Cleavage furrow occurs in the plane of metaphase plate, right angle to the long axis of the mitotic spindle
• Aster is responsible for cleavage furrow position
• contractile ring: assembles in the early anaphase (actin & myosin II) myosin dephosphorylation triggers cytokinesis
• Midbody: bridge between two cells, contains polar MT
• organelles partitioned with no special mechanisms mitochondria, chloroplasts; grow, fission -> # doubles ER, Golgi; fragmentation, vesiculation -> even distribution
• unequal segregation of cell components C. elegans “p-granules” to posterior -> form germ line cells
(independent to MT, but dependent on actin filament) styela yellow cresent (myoplasm) to vegetal -> form muscle (microfilament first phase, MT second phase)
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