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Tamarin: Principles of Genetics, Seventh Edition
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III. Molecular Genetics
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16. Gene Expression: Control in Eukaryotes
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The McGraw Hill Companies, 2001
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Gene Expression: Control in Eukaryotes
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technique has been developed that allows investigators to differentiate all of our chromosomes very quickly and accurately by seeing them painted in different uorescent colors. This technique allows a scientist or clinician to determine quickly whether any chromosomal anomalies exist, either in number (aneuploidy) or structure (deletions, translocations). The technique, chromosomal painting, is a
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variant of the technique known as uorescent in situ hybridization (FISH), in which a uorescent dye is attached to a nucleotide probe that
then binds to a speci c site on a chromosome and makes itself visible by uorescence (see g. 13.41). A whole chromosome can be made visible by this technique if enough probes are available to mark enough of the chromosome. However, there are not enough uorescent markers known to paint all 24 of our chromosomes (autosomes 1 22, X, Y) a different color. Now, with as few as ve different uorescent markers and enough probes to coat each chromosome, it is possible to make combinations of the different marker dyes so that each chromosome uoresces a different color. Because the colors are not generally distinguishable by the human eye, they have to be separated by a computer that then assigns each chromosome its own color. As gure 1 shows, the technique works very well. With it, we can rapidly determine any chromosomal anomaly in a given cell. This technique is helpful in clinical diagnosis of various syndromes and diseases, including cancer.
Figure 1 Chromosomal spreads after treating with probes speci c for all human chromosomes and attached to ourescent tags. Colors are generated by computer. Left (a, b) are the spread and karyotype of a normal cell; right (c, d) are the same for an ovarian cancer cell with complex chromosomal anomalies.
(Courtesy of Michael R. Speicher and David C. Ward, The coloring of cytogenetics, Nature Genetics, 2:1046 48, 1996, gs.
2 and 3. Photos courtesy David C. Ward.)
ensues. The rst tumor-suppressor gene to be isolated was the gene for retinoblastoma, a tumor of retinoblast cells, which are precursors to cone cells in the retina of the eye. This is a disease young children contract, because after the retinoblast cells differentiate, they no longer divide and apparently can no longer form tumors. The disease occurs both in a hereditary and a sporadic form. Both forms are presumably due to the recessive homozygous state of the locus. In the hereditary form, individuals inherit one mutant allele; a second mutation results in the disease. In the sporadic form, with identical
symptoms, both alleles have apparently mutated spontaneously in the somatic tissue of the retina.The retinoblastoma gene has also been implicated in other cancers, including sarcomas and carcinomas of the lung, bladder, and breast. How do we know that retinoblastoma results from the loss of suppression rather than simply the activity of an oncogene J. Yunis, who examined cells from several retinoblastoma patients, found a frequently deleted part of chromosome 13, speci cally band q14. Yunis noticed that the exact points of deletion varied from individual to
Tamarin: Principles of Genetics, Seventh Edition
III. Molecular Genetics
16. Gene Expression: Control in Eukaryotes
The McGraw Hill Companies, 2001
Cancer
individual, indicating that the phenomenon was due to loss of gene action rather than enhancement of gene activity due to the new placement of genes previously separated by the deleted material. Under normal circumstances, the retinoblastoma protein, RB, inhibits the cell cycle from advancing. If the appropriate checkpoint is passed, RB is phosphorylated by cyclin-dependent kinase and cyclin complexes, and the cell cycle progresses. As the protein product of a homozygous recessive mutant, RB no longer inhibits the cell cycle advance, even if the checkpoint has not been cleared. Thus, DNA-damaged and cancerous cells are allowed to continue to grow. The retinoblastoma gene has been isolated and cloned. The gene speci es a 105-kilodalton protein (p105) found in the nucleus, as would be expected if it were a suppressor of DNA transcription. It binds with at least three known oncogenic proteins: the E1A protein of adenovirus, the SV40 (a simian virus) large T antigen, and the 16E7 protein of human papillomavirus, a virus associated with 50% of cervical carcinomas. The implications are that these three viruses may use a similar mechanism in transformation, and this mechanism involves inactivation of the retinoblastoma p105 protein. Further support for the existence of tumorsuppressor genes came from work by E. Stanbridge and his colleagues with another childhood cancer, Wilm s tumor. This is a kidney cancer that is also believed to be caused by loss of action in a tumor-suppressor gene. It is associated with the loss of band p13 on chromosome 11. Researchers introduced a normal chromosome 11 into Wilm s tumor cells growing in culture. The result was normal cell growth, exactly what we would predict if the introduced normal gene were a tumor-suppressor gene. A third tumor-suppressor gene is the p53 gene, named for its 53-kilodalton protein product and located on chromosome 17. This gene is the most common mutation in cancers, found in more than 50% of human tumors. It achieved the status of Science magazine s 1993 Molecule of the Year. Since the p53 protein is found in so many cases, it is clear that its role as a tumor suppressor was of great importance in the normal activity of cells. Normally, p53 is highly unstable: the MDM2 protein binds its amino terminal end and ubiquinates it, leading to the rapid degradation of p53 in the proteasome within several minutes. However, p53 is stabilized when it is phosphorylated by cell-cycle checkpoint kinases. For example, ATM binds to double-stranded DNA breaks. Bound this way, it activates the protein CHK2, a checkpoint kinase that then phosphorylates p53. In the active state, p53 is a transcription factor that induces at least thirtyfour different genes, genes involved either in stopping the cell cycle, inducing apoptosis, or regulating itself. First, p53 stops the cell cycle to give the cell a chance to repair its DNA. Cell growth is arrested by the induction
(also called upregulation) of cyclin-dependent kinase inhibitors (proteins such as p21, WAF1, and CIP1). This action stops the cell cycle. In fact, if DNA repair does not take place, cells can be forced to remain permanently in G1 phase. Alternatively, p53 can induce cell death by upregulating the bax gene. Its protein is involved in the pathway to induce caspases, proteinases that destroy the cell. (Caspases get their name from the fact that they are cysteine-requiring aspartic acid proteinases. The bax gene s name comes from bcl-2 associated-x gene; bcl-2 is from B-cell leukemia/lymphoma-2.) Finally, the p53 protein is a transcription factor for the gene for MDM2, the protein that regulates p53. Thus, the p53 protein has a narrow window in which to stop the cell cycle or induce apoptosis, giving the cell a chance to repair its DNA damage or commit suicide. After this, the p53 protein is itself repressed ( g. 16.27). It is clear that the loss of p53 activity allows DNA damage to build up in a cell. This is why more than 50% of cancers involve loss of p53 activity. More than twenty other tumor-suppressor genes are known.
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