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Lecture 19

Lecture 19: "Gene Mutation"

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Department
Biology
Course
Biology 1002B
Professor
Tom Haffie
Semester
Fall

Description
Biology Lecture No. 19: Gene Mutation Monday March 19 , 2012 - + Mechanisms For His Reversion To His In Ames Test: -Lecturer Tom Haffie used the Ames test to find mutagens in wine. The system of study was based on - salmonella bacteria, which already had mutants that could not make their own histidine (His ). In a minimal medium (lacking in histidine) these mutant cells cannot survive. + -Throughout the duration of the Ames test, some of the mutant cells revert back to the normal His genotype. This reversion from mutant to normal genotype is still a mutation. Such reversion is upon which the Ames test is based since in a minimal medium, spontaneous revertants are only present in the wild type. -Small amounts of histidine are essential in the medium in order to allow the mutants to divide, but about 30 of them are able to actually grow and survive. For most mutation to occur, replication is required. When known mutagens are added to the medium, there is a dramatic increase in the frequency of reversion. The Ames test gives chemicals that are positive or at least suspect. Mutation: -A mutation is a heritable change in a double-stranded DNA sequence. A change in DNA that is not double-stranded is not a mutation, it is known as genetic damage. Common forms of change in the DNA sequence includes: base substitutions and insertion/deletion (“indel”) reorganization. Tautomeric Shifts & Base-Pairing: -The hydrogen bonds that are made by any nucleotide are not particularly stable. Hydrogen bonding arises from the distribution of electrons, which can shift spontaneously and give rise to tautomers through tautomeric shifts. -Why aren’t these changes in hydrogen bonding, called tautomeric shifts, causing mass genetic damage? It is due to the fact that these shifts rarely occur. The reality is that the assigned conventional base- pairings (AT, CG) are the most stable forms observable. However deviations from standard base-pairing (AC, GT) occur quite frequently and are spontaneous. Enzymes cannot tell these two forms of base- pairing apart. Transition Mutations: -A mismatch is a form of DNA damage and is not a form of mutation. A transition mutation is where a purine is replaced by another purine or a pyrimidine is replaced by another pyrimidine on both strands. A transversion mutation is just the opposite, where a purine is replaced by a pyrimidine and/or a pyrimidine is replaced by a purine on both strands. -Tautomeric shifts lead to mutation, but only after two rounds of replication. Mutagens As Tautomerically Unstable Analogues: -5-bromouracil is an analogue for thymine as DNA polymerase cannot tell the difference between this molecule and thymine. 5-bromouracil is incredibly unstable as it constantly switches its pairing partner and how many hydrogen bonds it contains. -If 5-bromouracil was a part of a particular DNA and suffered a tautomeric shift, it would call for a guanine molecule. -The effect of such a substitution as 5-bromouracil for thymine would depend on the complementary codon in the sequence. Codon Sequence & Amino Acid Sequence: -As the codon sequence correspond to the amino acids sequence, a change mutation in the transcribed DNA strand would have certain implications for the respective protein. -For example, if a A-T pair is replaced by a G-C pair, it may impact the polypeptide of that derives from that particular sequence. Silent Mutations: -If a mutation results in a codon that does code for the same amino acid, then it can be the result of a silent mutation since it does not change the efficacy of the polypeptide’s 3-D shape. Cells have the ability to absorb mutations or changes in DNA and RNA, but not in proteins. Missense Mutations: -If a mutation results in a codon that codes for different amino acid than the one intended, then it can be the result of a missense mutation since it changes the efficacy of the polypeptide’s 3-D shape. This change may or may not be dramatic on the phenotype depending on the circumstances. Nonsense Mutations: -If a mutation results in a codon that codes for a stop codon, then it can be the result of a nonsense mutation since it halts translation of the mRNA sequence into protein. This change induces a dramatic effect on the phenotype as the intended protein is not even completely synthesized. In/Del Mutation Mechanism: -In/del mutations tend to be sequence specific in that there are certain DNA sequences that more frequently lend themselves to in/del mutations (such as a “string” of thymines). Due to the string of adenine-thymine pairs, the newly synthesized DNA strand can “slip” during replication, causing a shift that essentially knocks out a thymine from base-pairing with adenine. -This small shift in the reading frame confuses DNA polymerase, which will actually replace the spot left by the misplac
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