3.A.2 Cell Division Part I The Cell Cycle and Mitosis In eukaryotes, heritable information is passed to the next generation via processes that include the cell cycle and mitosis or meiosis plus fertilization.
The cell cycle is a complex set of stages that is highly regulated.
Interphase is the stage of the cell cycle when the cell is not dividing.
Interphase consists of three phases: G1: Gap 1, during which the cell grows and functions normally. S: Synthesis, during which the DNA is replicated. G2: Gap 2, during which the cell continues growing and prepares for mitosis.
Mitosis is the stage of the cell cycle when the nucleus of the cell divides. Mitosis passes a complete genome from the parent cell to daughter cells.
Cytokinesis is the division of the cytoplasm and its contents Cytokinesis is the division of the cytoplasm and its contents. Mitosis followed by cytokinesis produces two genetically identical daughter cells. Cytokinesis in animal cells is accomplished by the formation of a contractile ring and a cleavage furrow as the cell is squeezed in the middle by elements of the cytoskeleton.
In plant cells, the rigid cell wall prevents the formation of a cleavage furrow. Instead, vesicles form along a cell plate. The vesicles fuse, forming new cell membrane.
The cell cycle is directed by internal controls or checkpoints The cell cycle is directed by internal controls or checkpoints. Internal and external signals provide stop-and-go signs at the checkpoints.
The G1 checkpoint decides whether the cell will divide, delay division or enter a resting stage (G0).
Often called the “restriction point”…seems to be the most important Often called the “restriction point”…seems to be the most important. If a cell does not pass this point, it usually goes to G0.
Most human body cells are in G0 Most human body cells are in G0. Cells can exit G0 when they receive the right signals.
The G2 checkpoint determines if the DNA has been successfully replicated and decides whether the cell is ready to proceed into mitosis.
The M checkpoint occurs during metaphase of mitosis and determines if all chromosomes are correctly aligned on the metaphase plate. This determines whether the cell is ready to proceed with cytokinesis.
Regulation of Checkpoints The G1 (G1 to S) and G2 (G2 to M) checkpoints regulated by cyclins and CdKs. The M checkpoint is regulated by the proper alignment of chromosomes in metaphase.
Wrap Up of Today’s Information:
MPF forms when a cyclin-dependent kinase (Cdk) is activated by a cyclin (they bind). This promotes mitosis.
CdK + Cyclin = maturation (or mitosis) promoting factor (MPF) Kinases are enzymes that phosphorylate things (which activates or deactivates them). Cyclin-dependent kinase: won’t work unless cyclin is attached, activating it. Always present in cells. Cyclin: a protein that activates a CdK by attaching to it. Cyclins are made and degraded as needed. CdK + Cyclin = maturation (or mitosis) promoting factor (MPF)
Only when MPF accumulates past a certain threshold level will the cell proceed from G2 checkpoint into mitosis.
How MPFs work: Cyclin concentration builds up in the cell throughout interphase. Cyclin binds to CdK and forms MPF. When enough MPF accumulates, G2 phase ends/mitosis begins.
How MPFs work: MPF degrades cyclin, lowering its concentration. (the cdk sticks around) After mitosis, cyclin begins accumulating again in the daughter cells.
Besides checkpoints, other signals that affect cell division include: - Growth factors - Density-dependent inhibition - Anchorage dependence
Growth factors are proteins released by specific cells that stimulate other cells to divide. An example is PDGF.
PDGF is associated with fibroblasts (blood clotting) PDGF is associated with fibroblasts (blood clotting). Without the release of PDGF, cells will not grow to repair tissues.
Other regulators include density-dependent inhibition (if it’s crowded, division stops) and anchorage dependence (will not divide unless attached to a substratum).
Cancer results from disruptions in cell cycle control Cancer results from disruptions in cell cycle control. Because of this, cancer cells reproduce at a rate far faster than normal cells, often forming a mass or tumor.
Cancer cells lack density-dependent inhibition and anchorage dependence. There are other key differences, which you will look at on your own.
Wrap up of the cell cycle http://www.cell-action.com/cell_cycle/cell_cycle.html