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Cytoplasmic signals…
chemicals (relay proteins, kinases, etc. in pathways) in the cell regulate cell cycle
Physical signals..
density dependent inhibition (as density increases amount of nutrients decreases slowing growth)
anchorage dependence (must be attached to divide; connection between substrate and plasma membrane and cytoskeleton)
fusing cells at two different phases of the cell cycle makes the molecules present in the cytoplasm of cells in S or M phase control the progression of the phase.
Cell Cycle Control System…
molecules in the cell trigger and coordinate key events in the cell cycle
G1 checkpoint…
a signal must be received to proceed through the process and then proteins are made to help synthesize dna
no signal = exit the cell cycle and enter G0
G2 checkpoint…
checks for mutations in dna
G0…
non-dividing state
mature nerve and muscle cells never divide
cells like liver cells exist in G0 until growth factors (due to injury) are present
significance: prevents the over accumulation of cells throughout the body; allows the organism to replace dead or damaged cells as needed.
M (metaphase) checkpoint…
checking to see if there are spindle fibers to each side and pole of the sister chromatids to prevent the entire chromosome from being pulled in one direction
Protein Kinase…
enzyme that transfers phosphate from ATP (converting it to ADP) to a protein
changes confromational shape, changing its function; activate or inactivate a protein
de/phosphorylation caused by protein kinases regulates the cell cycle (mitosis)
abnormalities can cause abnormal cells growth, contributing to the development of cancer
Cyclins (cytoplasmic signals)
class of proteins like enzymes
proteins that cyclically fluctuates concentration in cell cycle
binds/activate kinases to regulate cell cycle
cycling concentrations rise in cell during G1, S, G2 = they bind to and activate protein kinases called cyclin dependent kinases (CDKs)
M Phase Promoting Factor (MPF)…
a specific cyclin dependent dependant kinase that triggers the cell’s passage past G2 checkpoint into M phase.
triggers events like chromatin condensation, nuclear envelope breakdown, and spindle formation
G2 Checkpoint (Cyclins and Cyclin Dependent Kinases)…
synthesis of cyclin begins in S phase and accumulates
cyclin (key regulatory protein that controls cell cycle, binds to CDK) + CDK (type of protein kinase) = producing MPF, initiating mitosis (pass G2 checkpoint)
Each MPF promotes mitosis by phosphorylating proteins…
hundreds of different MPF molecules that act on different cellular structures
example: phosphorylates proteins in nuclear envelope to cause fragmentation or phosphorylates tubulin protein to cause the formation of the spindle fibers
significance: all necessary MPF molecules must be present and activated to achieve two genetically identical daughter cells
Internal Signals - Regulation of Anaphase…
does not occur until all the chromosomes are attached to the spindle at the metaphase plate
kinetchores send a molecular signal that causes the sister chromatids to remain together delaying anaphase while motor proteins remain inactive
significance: prevents daughter cells from having extra or missing chromosomes
External signals - Growth Factors…
proteins released by certain cells that stimulate other cells to divide
example: platelet-derived growth factors (PDGF) produced and released by blood cells called platelets results in the growth of fibroblast cells. these cells have PDGF protein receptors on cell surface and once they bind together, the cell passes G1 checkpoint and divides (increasing production of cyclin).
significance: there are over 50 different external growth factors that can trigger cells to divide.
Cancer cells…
cancer cells lose both density dependent inhibition and anchorage dependence
Benign…
abnormal cells remain at the original site
doesn’t affect organic function
Malignant…
invasive and impairs the function of one or more; results in cancer
excessive proliferation, can have abnormal numbers of chromosomes, can have a disabled metabolism
Metastasis…
cancer cells move from their original location to other sites in the body