Although most mutations are either neutral or harmful they are also the raw material for evolution. Such mutations from alleles, alternate forms of a given gene that may produce differences in structure or function such as black, brown or blond hair in humans, or different mating calls in frogs.
Stages of Mitosis~
2)Chromosomes make identical copies of themselves.
3)They line up along the centre.
4)They move apart.
5)Two daughter cells form with identical chromosomes to the parent cell.
Homologous chromosomes have the same genes, but each homologue may have the same alleles of some genes and different alleles others.
The cell cycle is tightly controlled. Both during the embryonic development and during the maintenance and repair of the adult body, progressing through the cell cycle is regulated primarily by two interacting processes. (1)Production of, and responses to, growth factors that generally speed up the cell cycle; (2)Intracellular checkpoints that stop the cell cycle if problems such as mutations in the DNA or misalignment of the chromosomes have occurred. Most cancers develop because one of both of these processes goes awry.
Many different molecules control the cell cycle;
Porto-oncogenes:Any gene whose proteins tends to promote mitotic cell division if called a proton-oncogene. The genes for growth factors, grow factor receptors, and some cyclins and Cdks are proton-oncogenes. In most cases, progress through the cell cycle beings when a growth-stimulating protein such as epidermal growth factor (EGF) binds to a receptor on the surface of a cell. This stimulates the synthesis of cyclins which bind to Cdks and activate them. Thus, these proton-oncogenes are essential to the normal control of the cell cycle. Tumor suppressor genes:The protein products of tumor suppressor genes prevent uncontrolled cell division and the production of daughter cells with mutated DNA, both of which are common in tumors. Cdks regulate the activity of other proteins by adding a phosphate group to them.
One such protein is Rb. Normally, Rb inhibits transcription of several genes whose protein products are required for DNA synthesis. Phosphorylation of Rb by Cdks relieves this inhibition in the G, phase of the cell cycle, allowing the cell to proceed to the S phase and replicate its DNA. This chain of events, from growth faction stimulation to phosphorylation of Rb, ensures that the cell cycle starts up only when the body needs it to. Another tumor suppressor protein, called P53 monitors the integrity of the cell’s DNA and indirectly regulates Rb activity.
Healthy cells with intact DNA, contain little P53. However, when DNA has been damaged (for example by ultraviolet rays in sunlight), P53 levels rise. The P53 proteins that inhibit Cdks. If Cdks are inhibited then Rb is not phosphorylated and DNA synthesis is blocked; this prevents the cell from producing daughter cells with damaged DNA. The P53 stimulated the synthesis of DNA repair enzymes. After the DNA has been repaired, P53 levels decline, Cdks become active, Rb becomes phosphorylated and the cell enters the S phase. If the DNA cannot be repaired, P53 triggers a special from of cell death called apoptosis, in which the cell cuts up its DNA and effectively commits suicide.