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8 Cards in this Set
- Front
- Back
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How do InDel mutations form? |
slipped mispairing of repeated sequences |
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what is a splice site mutation? |
mutation that occurs during the processing of pre-mRNA that affects the way the pre-mRNA splices - specific intron splicing sites |
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what effects on mRNA processing can occur due to mRNA mutations? |
the activity of the spliceosome is altered - it's binding site recognition may become inaccurate: *exonic deletion (skipping) *intronic inclusion *cryptic splice site activation (partially cut exons) |
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describe fwd and rvrs mutations |
forward mutations: wild type -> mutant reverse mutations-> exact reversion (true genotypic)/ equivalent reversion (diff sequence, but producing wild type AA seq.) |
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Describe how base ionisation leads to mutations |
*base analogue can be incorporated into seq. (e.g. bromine instead of methyl) with normal function *when changing ionisation state, analogue will imitate a transition mutation, pairing with different NT (ionisation usually due to mutagenic activity) |
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what is the basis behind wobble base pairing? |
the third position on the anticodon is more relaxed than the first and second. the mRNA / tRNA pairing is less strict allowing for higher degeneracy in the code: amino acids may be specified by more than one codon. within an open reading frame, the resulting AA is likely to be synonymous |
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What mutation do the mutagens ethylmethylsulfonate (EMS) and nitrosoguanadine (NG) induce and how? |
*EMS adds ethyl group to Guanadine, which makes it bind to Thymine - GC to AT transitions
*NG adds methyl group to Guanadine or Thymine, causing GC to AT transitions |
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What is the mutation caused by Hydroxylamine? |
adds OH group - hydroxylation - to Cytosine, making it base pair with Adenine, causing CG to AT transitions |
