The Cell Cycle Decide whether each of these statements is true or false, and then explain why 1.

Since there are about 1013 cells in an adult human, and about 10 10 cells die and are replaced each day, we become new people every three years. FA S! "#ot all are replaced at the same rate$ neurone and heart muscle cells are rarely replaced, blood % &ut cells are replaced re&ularly' (. Althou&h the len&ths of all phases of the cycle are variable to some extent, by far the &reatest variation occurs in the duration of )1. *+,! ")1 is critical because protein is synthesis in preparation of S-phase. .n )1, there/s a chec0point to chec0 whether the external environment and internal environment whether replication is favorable1viable or not' 3. *he re&ulation of cyclin-2d0 complexes depends entirely on phosphorylation and dephosphorylation. FA S! "+e&ulation of activity not only involve phosphorylation1dephosphorylation, but also 2D3 inhibitor' 4. .n order for proliferatin& cells to maintain a relatively constant si5e, the len&th of the cell cycle must match the time it ta0es for the cell to double in si5e. *+,! 6. *he six sta&es of 7 phase-prophase, prometaphase, metaphase, anaphase, telophase, and cyto0inesis-occur in strict se8uential order. *+,! 9. Serum deprivation causes proliferatin& cells to stop where they are in the cell cycle and enter )0. FA S! ":nly if conditions are not met, cell exit cell cycle and enter )0' ;. <uddin& yeast and mammalian cells respond to D#A dama&e in the same way= they transiently arrest their cell cycles to repair the dama&e and if repair cannot be completed, they resume their cycles despite the dama&e. FA S! Problems 1. .f the most basic function of the cell cycle is to duplicate accurately the D#A in the chromosomes and then distribute the copies precisely to the dau&hter cells, why are there &aps between S phase and 7 phase> to prepare the cell for cell division to chec0 for errors double the amount of protein and or&anelle cell need to monitor internal and external environment so that it is favourable for mitosis

(. .t is remar0able that the concentration of cyclin < in the cleavin& clam e&& rises very slowly and steadily throu&hout the cell cycle, whereas 7-2d0 activity increases suddenly at mitosis. See Fi&ure below. ?ow is the activity of 7-2d0 so sharply re&ulated in the presence of a &radual increase in cyclin <> *he 0inase @ee1 phosphorylate the cyclin<1csc( complex, remain inactive 2dc(6 dephosphorylate , activate cyclin<1cdc(, &( proceed to mitosis phase 2dc( Aoined with cyclin < formin& cyclinb1cdc( complex, wee1 phosphorylate the complex hence it will become inactivate, ca0 also phosphorylate the complex. *he complex build up &radually, cdc(6 dephosphorylate the inhibitory protein$ activate the complex which &ive positive feedbac0$ inhibit wee1 from phosphorylatin& the earlier complex. Active complex also &ive positive feedbac0 to cdc(6 to activate more of the complex build up.

*he rise and fall of 7-2d0 activity and cyclin < concentration durin& cell cycle in a cleavin& clam e&&. 3. Describe each phases in the cell cycle. )1 B 2ell will monitor the environment, protein synthesis need for s phase, the interval between mitosis and D#A replication characteri5ed by cell &rowth centrioles replicate, S B D#A replication occurs )( B Second &rowth phase in preparation for cell division, chec0point mechanism ensure cell is ready for mitosis, protein synthesis 7itosis B prophase, metaphase, anaphase, telophase, cyto0inesis )0 B restin& state, only &1 can &o bac0 to &0 4. Describe the normal )11S phase transition and events which prevent the pro&ression of this sta&e of the cell cycle. *ransition that occurs at restriction point "+' commits the cell to the proliferative phase

.f conditions are not met, cell exit cell cycle and enter )0 "non-proliferative phase where &rowth, differentiation and apoptosis occur' 2ell will monitor its environment "external % internal' and si5e. :nce the time is ri&ht, cell will carry on with D#A replication and cell division !vent which prevent the pro&ression of cell cycle$ D#A dama&e caused by radiation p63 will accumulate, inducin& p(1-mediated inhibition of cyclin !12D3 and cyclin D12D3 7dm( then inactivate p63, which subse8uently inactivate p(1 *)F-C receptor is then activated and inhibits cyclin D12D3 further by p16 2yclic-A7D inhibit cyclin D12D3 complex via p(; E2yclin D12D3 is the 0ey complex at the be&innin& of the cell cycle Additional info= #ormal transition and pro&ression Activation of cyclin D12D3 complex Dhosphorylation of retinoblastoma p-+b dissociate from !(F "a transcription factor' !(F then drives the transcription "D#A synthesis in S-phase'

6. Describe the normal )(17 phase transition and events that prevent the pro&ression of this sta&e of the cell cycle. #ormal )(17 phase transition 2D2(6 dephosphorylate cyclin <12D2( complex 2yclin <12D2( complex is then activated by phosphorylation of *hr190 "by 2A3, and before that 2A3 was activated by 2A3A3' and dephosphorylation of *hr16 "by 2D2(6 phosphatase' *he activation of cyclin <12D2( complex let the cell to proceed to 7-phase !vent which prevent the pro&ression of cell cycle$ 2h01 phosphorylate 2D2(6 2ausin& 2D2(6 to bind to protein 14-3-3 and become inactivated *herefore preventin& 2yclin <12D2( from dephoshorylation and the subse8uent activation mechanism