modified from a slide show by kim foglia
DESCRIPTION
MODIFIED from a slide show by Kim Foglia http://www.explorebiology.com/documents/37Ch12MitosisRegulation2005a.pdf. INTERPHASE = G 1 , S, G 2. G 2 - Gap 2 Grow Produce molecules & organelles needed for cell division. MITOSIS. G 1 - Gap 1 Grow by producing proteins & organelles. - PowerPoint PPT PresentationTRANSCRIPT
MODIFIED from a slide show by Kim Foglia http://www.explorebiology.com/documents/37Ch12MitosisRegulation2005a.pdf
INTERPHASE = G1, S, G2
G1- Gap 1Grow by producing proteins & organelles
G2- Gap 2Grow Produce molecules & organelles needed for cell division
S- SynthesisDNA replication
Some can return to cycle with signal (Ex; Liver cells respond to injury)Some never divide again (Ex: Mature nerve, muscle cells)
MITOSIS
G0- Cell leaves cycle and stops dividingMost body cells in this phase
Cyclin-dependent kinases (Cdk’s) are present all the time but inactive unless combined with cyclins
Presence of MPF triggers passage past G1 & G 2 checkpoints
KINASES-Enzymes that workby adding a phosphate groupto other molecules
Cyclin levels change throughoutcell cycle
Fluctuating levels of different Cyclin-Cdk complexesseem to control all stages of cell cycle
Telomeres protect DNA from being degraded
Telomeres become shorter with each replication; shorter in older cells
Telomerase enzyme lengthens telomeres
Cancer cells have increased telomerase activity
Jack Szostak Carol Greider Elizabeth Blackburn.
2009Nobel PrizePhysiology/MedicineDiscovery of Telomeres
Most cells divide 20-50 times in culture; then stop, age, die
Cancer cells are “immortal” -HeLa cells from a tumor removed from a woman (Henrietta Lacks) in 1951 are still reproducing in culture
http://www.sanger.ac.uk/Info/Press/gfx/081223_cells_300.jpg
CANCER CELLS• Don’t respond to control signals• Lose density-dependent inhibition• Lose anchorage dependence• Telomerase enzymes maintain/replace
telomeres
Transformation- process that changes a normal cell into a cancer cell