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AP Biology Chapter 12 Part 2

Terms in this set (9)

Cells divide for 3 reasons: reproduction, growth, repair and renewal.
Reproduction --reproduce asexually--one-celled organism use mitosis as a way of reproduction
Growth--cell division helps growth by taking you from a fertilized egg to a multi-celled organism
Repair and renewal -- replaces cells that die from normal wear and tear or from injury

Coordination of cell division in multicellular organisms is critical for normal growth, development and maintenance. Cells have an upper and lower size limit. If it was too small it would not contain all organelles. It can't be too big because of the ratio of the cell surface area to volume. An increase in size can result in a surface area too small for the adequate exchange of materials. Some cells must be large for a purpose To maintain a suitable size, growth and division must be coordinated, if a cell doubles in size the daughter cells will be too big or too small, this will happen with each generation and the cell will die. Coordination of cell growth and division is important for cells to stay the same size from generation to generation. Coordinating the timing of cell division, and rates of cell division so that all cells are not on the same cycle. This is important because if all cells were on the same cycle then you wouldn't have cells available for functions at all times. The frequency of cell division varies by cell type. (example embryos have a less than 20 minute cell cycle, skin cells every 12-24 hours, liver cells once every 1-2 years, mature nerve and muscle cells not at all)

Control of cell division is important because too much cell division can cause mutation and overgrowth of cells resulting in cancerous growths. A multicellular organism uses:
Internal Controls to coordinate and control this division.
A multicellular organism must have MPF, which is Cdk and Cyclin put together. This turns on other proteins for mitosis.
External Controls to coordinate and control this division:
Growth factors -- coordination between cells, protein signals released by body cells that stimulate other cells to divide-- Positional Inhibition--Animal Cells must be anchored (attached to a substrate)to divide -- Also they cannot be too crowded ("Density Dependant Inhibition")- Crowded cells stop dividing. Each cell binds a bit of growth factor so that there is not enough activator left to trigger division in any one cell.
Cancer is essentially a failure of cell division control. It is unrestrained and uncontrolled cell growth.
Growth factors can create cancer -- proto-oncogenes normally activate cell division. When these genes become mutated and are permanently switched to an on position, they can cause cancer by continuous and uncontrolled division of cells. Tumor suppressor genes which normally inhibit cell division can be switched to an off position and tumors will grow uncontrollably causing cancer.
All cancers have to shut down p53 activity. Gene p53 plays a key role in the G1/S restriction point. p53 halts cell division if it detects damaged DNA -- it can stimulate repair enzymes to fix DNA, force cell into the G0 resting stage, keep cell in G1 arrest, cause apoptosis of damaged cell.

Development of Cancer occurs after a cell experiences 6 key mutations. 1- unlimited growth (turn on growth promoter genes) 2 - ignored checkpoints (turn off tumor suppressor genes -p53) 3-escape apoptosis (turn off suicide genes) 4- unlimited division (turn on chromosome maintenance genes) 5-promotion of blood vessel growth (turn on blood vessel growth genes) 6 - overcome anchor and density dependence (turn off touch-sensor gene)
Proto-oncogenes produce protein products that enhance cell-division or inhibit normal cell death. While, tumor suppressor genes make proteins that prevent cell division or cause cell death. Proto-oncogenes and tumor suppressor work together to regulate cell growth. The proto-oncogenes accelerate growth, while the tumor-suppressor genes slow cell growth. Mutations that produce oncogenes, the mutated form of proto-oncogenes, rapidly accelerate cell growth, while mutations that affect tumor suppressors prevent the normal inhibition of growth. Either of these cause uncontrolled cell growth.
An example of a mutated proto-oncogene is when RAS becomes mutated. RAS is another oncogene that normally functions as an "on-off" switch in the signal cascade. Mutations in RAS cause the signaling pathway to remain "on," leading to uncontrolled cell growth. About thirty percent of tumors, including many important systems, have a mutation in RAS. Most oncogenes are dominant mutations and single copies of this gene can be sufficient for the expression of this growth.
Mutations in tumor suppressor genes result in cells that no longer show normal inhibition of cell growth and division. Theses mutations result in a loss of function, so they are usually recessive. The trait can not be expressed unless both copies of the gene are mutated. An example of this mutated tumor suppressor gene is hereditary retinoblastoma, RB. RB is a serious retina cancer occurring in early childhood. When one parent carries the mutation, there is a fifty percent probability that the offspring will receive this mutation. Most likely the offspring that receives it will then produce a copy of mutated RB in the second gene. The individual then develops retinoblastoma.