O a base substitution in an intron 5' splice site O a frameshift in an exon O a missense in an exon O a base substitution in an enhancer region

The following is a polypeptide from a wild type organism:met – ser – tyr – his – trp – arg – ser – phe – aspA mutation of this polypeptide was isolated and its amino acid sequence was determined. Indicate the type of mutation that occurred and its on the amino acid chain.Mutant: met – ser – tyr – his Group of answer choices Deletion, missense Transversion, nonsense Transition, nonsense Transition, missense

When the sequence CpG occurs, the cytosine can be methylated. If a methylated cytosine is then deaminated, it will be mutated to       ["adenine", "thymine", "uracil", "guanine"]  . As a result, CpG sequences are underrepresented in the genome. The presence of a CpG island at a particular location suggests that the location might be a(n)       ["exon", "promoter", "enhancer", "intron", "telomere"]  . Pick answers within quotation marks to fill in the blanks.

When an EcoR1 fragment, which represents the coding region of a human gene X, is cloned into the EcoR1 site upstream of the coding region of a prokaryotic gene (such as GST) (i.e., to make a X-GST fusion protein), what is the chance of an in-frame fusion? Please draw a diagram to explain your answer. Do you need to delete the stop codon of the X gene coding region before fusing it to the GST coding region? Please draw a diagram to explain your answer. Notes: It is NOT known which strand of the human gene X is the template strand for transcription. 2) Both X and GST protein fragments must be produced correctly)

After comparing the whole genome sequencing results from a candidate that you suspect has a mutation that causes a downstream shift in start site selection to the parent strain to rule out pre-existing mutations, you are left with the following list of missense mutations.  In 100 words or less, explain which of these mutations you believe is likely responsible for the transcription-related defects observed in your candidate strain and why you have ruled out the others.SWH1 D338V TFA1 C127R PKC1 I866L

The following is a list of mutations that have beendiscovered in a gene that has more than 60 exons andencodes a very large protein of 2532 amino acids.Indicate whether or not each mutation could cause adetectable change in the size or the amount of mRNAand/or a detectable change in the size or the amountof the protein product. (Detectable changes in size oramount must be greater than 1% of normal values.)What kind of change would you predict?a. Lys576Val (changes amino acid 576 from lysineinto valine)b. Lys576Argc. AAG576AAA (changes codon 576 from AAG toAAA)d. AAG576UAGe. Met1Arg (at least two possible scenarios exist forthis mutation)f. promoter mutationg. one base pair insertion into codon 1841h. deletion of codon 779i. IVS18DS, G–A, + 1 (this mutation changes thefirst nucleotide in the eighteenth intron of the gene,causing exon 18 to be spliced to exon 20, thusskipping exon 19)j. deletion of the poly-A addition sitek. G-to-A substitution in the 5′ UTRl. insertion of 1000 base…

Geneticists often use the alkylating agent ethylmethane sulfonate (EMS; see Figure 15.6) to induce mutations in Drosophila. Why is EMS a mutagen of choice for genetic research? What would be the effects of EMS in a strain of Drosophila lacking functional mismatch repair systems?

Identify the best match between the mutation description and term.   a. Transversion: results in a change in single nucleotide from a purine to another purine or a pyrimidine to another pyrimidine   b. Nonsense mutation: a change in the DNA that changes the codon code from one amino acid to another amino acid   c. Missense mutation: causes a drastic change in phenotype because the change causes a premature stop in the amino acid sequence   d. Indel: has the potential to cause large changes in transcription and subsequence amino acid sequence due to reading frameshifts

A disease is caused by having no functional protein produced from the kip gene. An individual has this disease but has no mutation in the kip gene. You look at other gene candidates that could result in no functional kip protein. A gene called D5 codes for a methyltransferase that methylates the kip promoter region. A gene called T3 codes for an acetylase that acetylates the histones in the region of the kip gene. Fill in the following blanks. In the situation described above, in which no kip protein is made, it is likely that the D5 gene has a mutation that ___________ the D5 protein or that the T3 gene has a mutation that ___________the T3 protein.   Blanks can either be deactivates or activates

a. Why is it impossible to induce nonsense mutations(represented at the mRNA level by the triplets UAG,UAA, and UGA) by treating wild-type strains with mutagens that cause only A• G → T• C transitions in DNA?b. Hydroxylamine (HA) causes only G• C → A• T transitions in DNA. Will HA produce nonsense mutations inwild-type strains?c. Will HA treatment revert nonsense mutations?