Chapter 9
1. Mutations can be very negative in that it can cause cancer in somatic cells. However it is important to note that mutations will also lead to variability which is beneficial to us. Mutations in intergenic DNA affects regulations of protein products which is actually less detrimental than mutations in exons which code for the proteins.
2. Transition is the error that causes the base to change from a purine to purine or pyrimidine to pyrimidine. Transverses are base changes from pyrimidines to purines or purines to pyrimidines. The more common of the two is transitions because the base changes to a similar shaped nucleotide so the geometry is similar to the correct sequence.
3. Translocation between chromosome 9 and …show more content…
5-bromouracil (enol) will form a pair with guanine during replication. A second replication will then cause the new guanine to pair with cytosine. This is a transition mutation.
18. The Ames Test is used to determine potential carcinogenic effects of chemicals. This test uses S. typhimurium that cannot synthesize histidine. Mutagens are then added that causes missense or frameshift to fix the mutation and allow it to grow.
19. MutT is important because it helps in the degradation of base 8-Oxo-dGTP (oxoG). The base oxoG is able to form pairs with C and A. Cells that lack MutT are unable to remove oxoG which causes adenines to be replaced with cytosines because of their better geometrical pairing (C:oxoG).
20. DNA polymerase recognizes misincorporated base pairs by checking the geometry. Mismatches have 10X greater affinity for DNA polymerase 3’ 5’ exonuclease domain.
21. In mismatch repair, MutS scans the DNA for distortion. Distortion changes MutS conformation which allows it to recruit MutL to join the complex. MutL activates MutH which then cleaves/nicks DNA near mismatch.
22. Mismatch repair system interacts with the minor groove of DNA. They interact with the minor groove because this allows them to bind …show more content…
Translesion DNA synthesis is used only as a last resort. It involves using a DNA polymerase that recognizes dimers or unrepaired sites. Translesion polymerase theta is essential to the production of high-affinity antibodies.
37. Xeroderma pigmentosum increases cancer susceptibility to skin carcinomas. Xeroderma pigmentosum results from failure of the nucleotide excision repair.
38. Expansion are caused by cell division/DNA polymerase, transcription, and oxidative damage/repair. As one ages, he/she is exposed to these factors constantly.
39. Most cancer results from faulty DNA repair mechanisms.
40. Cells become cancerous from point mutations (CpG transition in p53), double-stranded breaks, major chromosome rearrangements, chromosome loss/gain, loss of checkpoints, activation of oncogenes, and turning off tumor suppressors via hypermethylations.
41. Mutations and chromosomal abnormalities will affect the regulation of proteins or the structure of the proteins. Regulation changes of proteins can cause diseases. Structural changes of proteins can cause diseases such as sickle cell anemia.
42. From the prostate cancer study, it was seen that cancers can exchange genes. The exchange of certain genes can result in the activation or repression of other genes.