Presentation on theme: "Chapter 20 Biology Sixth Edition Raven/Johnson (c) The McGraw-Hill Companies, Inc. 20.2 and 20.3 only."— Presentation transcript:
Chapter 20 Biology Sixth Edition Raven/Johnson (c) The McGraw-Hill Companies, Inc and 20.3 only
Mutations are rare (a particular gene typically mutates in about 1 in a million gametes) but important. One method of evolution. More important (in terms of evolution) in germ-line cells than in somatic cells. Why? Mutation in the bithorax – a gene important in a critical stage of development.
I love Biology 155 so much, I wish I could take it again. I live Biology 155 so much, I wish I could take it again. I take Biology 155 so much, I wish I could love it again. Point mutation Genetic Recombination Genetic recombination – alters gene location and can occur by gene transfer or reciprocal recombination Change in the content of a genetic message
DNA Alteration by Mutation Base substitution – Spontaneous pairing errors Chemical modification – a base is chemically altered by a mutagenic chemical DNA breaks – Ionization radiation can cause double strand breaks in DNA Slipped mispairing – frameshift mutation Triplet expansion – 3-base sequence repeated several times
Cancer is unregulated cell growth and results in a tumor – caused by damaged genes. Cells that leave a tumor and form new tumors at distant sites are called metastses.
Sarcoma – tumors arising from connective tissue, bone, or muscle. Carcinoma – tumors arising from epithelial tissue such as skin. Mutagen (mutagenic) – an agent responsible for causing a mutation in DNA. Carcinogen (carcinogenesis theory) – an agent thought to cause cancer.
- Has enzymes that can convert carcinogens to mutagens The more colonies – the more potent the carcinogen
Many cancers can be avoided just by altering our behavior!
Some Tumors are Caused by Chemicals - and many of these chemicals are common (see table 20.3): Benzene, diesel exhaust, mineral oils, pesticides, cigarette smoke!
Mutations in proto-oncogenes genes Proto-oncogenes are responsible for initiating cell division when the correct external signal is received (‘Simon says’). When they mutate to oncogenes, they initiate cell division without receiving external signals. Thus, this cell continues to divide without regulation (doesn’t wait for ‘Simon says’).
Mutations in tumor-suppressor genes Tumor-suppressor genes are responsible for blocking cell division (‘Simon didn’t say’). When they mutate to, they are no longer able to block cell division. Thus, this cell continues to divide without regulation (doesn’t wait for ‘Simon says’).
Phosphorylation of Rb releases E2F and stimulates cells division p16 binds with Cdk, blocking cyclins, so E2F is never released, reinforcing the G1 checkpoint. Mutations in tumor-suppressor genes
Damage to p53 stops this process.
It usually takes about four mutations within a cell to initiate cancerous growth. That is why cancer is more prevalent among the elderly. Exposure to carcinogens can greatly speed this process!
1) Receiving the signal to divide. 2) Relay switch. 3) Amplifying the signal. 4) Releasing the brake. 5) Checking that everything is ready. 6) Telomerase Also - Preventing Angiogenesis and Metastasis
Plasmid – extrachromosomal DNA segments Conjugation
When chickens are infected with this virus, the src viral gene doesn’t need the chicken promoters to initiate cell division.