BIOL 3208 Assignment #3 32 points 1. Below is a figure of the rII map based on the Crick et al XXXXXXXXXXpaper. For the purpose of this assignment, assume that the “unacceptable regions” do not exist....

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BIOL 3208 Assignment #3 32 points 1. Below is a figure of the rII map based on the Crick et al. (1961) paper. For the purpose of this assignment, assume that the “unacceptable regions” do not exist. All “-” strains mutations are above the blue line, all “+” strains, below. a. Fill out the following table as to what phenotype (wt for wild-type, or rII for rII) would be expected with the double and triple mutants, assuming a triplet, nonoverlapping, commaless code. 5 points Mutant 1 Mutant 2 {Mutant 3} Phenotype FC(82) FC(63) n/a FC(38) FC(21) n/a FC(58) FC(0) n/a FC(41) FC(21) FC(58) FC(86) FC(88) FC(87) b. Now imagine, if you will, an alternate universe, where Frances Crick, completed the same work, only found the results below (using the same map and point mutants). What can you conclude about the code in this universe?2 points Mutant 1 Mutant 2 {Mutant 3} {Mutant 4} Phenotype FC(0) FC(40) FC(63) n/a rII FC(88) FC(0) n/a n/a wt FC(21) FC(58) n/a n/a wt FC(0) FC(63) FC(58) FC(41) wt c. Knowing the genetic code now, what are the odds that an insertion would have damaged the start codon of a gene, resulting in a null mutant that could not be suppressed by a subsequent deletion? Assume the gene is 999 bp, including the start and stop codons. Show your work.3 points d. Knowing the genetic code now, what are the odds that an indel would have damaged a gene by creating a premature stop codon, resulting in a null mutant that could not be suppressed by a second indel? Assume: i. that the gene is 999 bp and any premature stop would result in a loss of function ii. that the codon usage and polypeptide is essentially random. iii. that the mutagen will cause an insertion or deletion equally and random iv. If an insertion, the inserted base will also be random You’ll want to refer to a codon table for this problem. In addition to online, there is one on page 471. For example, the odds of getting a UGA stop by an insertion: inserting a U in front of GA somewhere along the gene would be (1 in 2) to get an insertion instead of deletion and; (1 in 4) for getting a U inserted instead of a G, C, or A) and; (1 in 4) for G and (1 in 4) for A in the adjacent positions. This is (0.5)x(0.25)x(0.25)x(0.25): 0.0078 or 0.78% for any one indel event. If we accept this might happen anywhere along the length of the gene, of the 993 indels that might happen, only ~7 would result in a premature UGA stop from an insertion event (the start and stop codon are removed, since mutation of either of those wouldn’t be a premature stop mutation). That accounts for one way to get a stop codon, how many others are there?6 points 2. The genetic code is “degenerate” (degenerate: another term chosen arbitrarily by F Crick that we continue to use to this day), or more accurately, it has redundancy. There are more codons than amino acids, thus one amino acid can be coded for by more than one codon. a. There is a phenomenon known as codon usage bias. What is codon bias? Find and cite a reliable source to explain this.3 marks b. What significance does this have for biotechnological applications like engineering organisms with genes from other organisms?2 marks 3. Of the scientists we have read about so far (up to and including Chp 5), who seems to be the most skeptical of new ideas/hypotheses? Support your answer with evidence from the text.5 marks 4. Long before the genetic code was determined, the identification of amino acids in cells was a popular field of research. When Watson and Crick sat down to propose a list of amino acids that would be coded for (and everything else assumed to be enzymatically modified, after protein synthesis), there was over 25 amino acids found in proteins. Watson and Crick settled on 20, and it so happens that they chose the 20 that are determined by the genetic code. How much of their good fortune was plain stupid luck and how much was clever reasoning? Support your argument with appropriate references to the text (Chp 5).5 points 5. Watson spent many months trying to describe RNA structure. Why do you think RNA was so much harder to get meaningful data from X-ray crystallography?2 points 6. A student believes that they have mapped their unknown Fastplant mutant to a marker locus. They have produced the following results from observing 30 F2 progeny that were homozygous recessive for the mutation: Heterozygous Homozygous FF Homozygous RR Total 8 plants 18 plants 4 plants 30 plants a. Using a chi-square test, determine if there is a reasonable likelihood (i.e. that the probability that the variance from a 1:2:1 ratio is less likely than 5%) that this data supports the student’s hypothesis. Show your work.3 marks b. If the gene is most likely linked, what is the gene distance in cM? Show your work.2 marks Untitled-1 © 1961 Nature Publishing Group © 1961 Nature Publishing Group © 1961 Nature Publishing Group © 1961 Nature Publishing Group © 1961 Nature Publishing Group © 1961 Nature Publishing Group
Answered 3 days AfterNov 11, 2021

Answer To: BIOL 3208 Assignment #3 32 points 1. Below is a figure of the rII map based on the Crick et al...

P answered on Nov 15 2021
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BIOL 3208 Assignment #3 32 points    
1. Below is a figure of the rII map based on the Crick et al. (1961) paper. For the purpose of this assignment, assume that the “unacceptable regions” do not exist. All “-” strains mutations are above the blue line, all “+” strains, below.
    
a. Fill out the following table as to what phenotype (wt for wild-type, or rII for rII) woul
d be expected with the double and triple mutants, assuming a triplet, nonoverlapping, commaless code.     5 points
    Mutant 1
    Mutant 2
    {Mutant 3}
    Phenotype    
    FC(82)
    FC(63)
    n/a
    wt
    FC(38)
    FC(21)
    n/a
    wt
    FC(58)
    FC(0)
    n/a
    rII
    FC(41)
    FC(21)
    FC(58)
    rII
    FC(86)
    FC(88)
    FC(87)
    wt
b. Now imagine, if you will, an alternate universe, where Frances Crick, completed the same work, only found the results below (using the same map and point mutants). What can you conclude about the code in this universe?    2 points
    Mutant 1
    Mutant 2
    {Mutant 3}
    {Mutant 4}
    Phenotype    
    FC(0)
    FC(40)
    FC(63)
    n/a
    rII
    FC(88)
    FC(0)
    n/a
    n/a
    wt
    FC(21)
    FC(58)
    n/a
    n/a
    wt
    FC(0)
    FC(63)
    FC(58)
    FC(41)
    wt
All the living organisms share the same genetic code showing the evolutionary history. The genetic code is read with three bases at a time.
Hence, the mutations, results in the alterations of reading the genetic code and the same was represented in the table.
There will be shift in the reading frames of the hence, there will be the changes in the final phenotype.
c. Knowing the genetic code now, what are the odds that an insertion would have damaged the start codon of a gene, resulting in a null mutant that could not be suppressed by a subsequent deletion? Assume the gene is 999 bp, including the start and stop codons. Show your work.    3 points
In ability to gene transcription into mRNA or it’s the in ability of the mRNA to translate into the protein. In case of start codon mutation, the mutates mRNA would be shunted to the ribosomes, but the translation would not take place. This is because an initiation codon is responsible for staring translation not transcription. Hence it cannot necessarily produce proteins as this codon lacks a proper nucleotide sequence that can act as a reading frame.
Example:
999 bp means- total 333 codons will be there UGC- cystine codon
UAA,UAG,UGA
If the mRNA made up of
UGU, UGU, UGU…………………………..UGU, UAG = codes for cysteine polypeptide.
A
Insertion of A in between the G and U of the start codon will result in the stop codon
UGA, UUG, UUG………………….UUG, UUA, = the cysteine polypeptide synthesis will be inhibited at the stating only.
d. Knowing the genetic code now, what are the odds that an indel would have damaged a gene by creating a premature stop codon, resulting in a null mutant that could not be suppressed by a second indel? Assume:
i. that the gene is 999 bp and any premature stop would result in a loss of function
ii. that the codon usage and polypeptide is essentially random.
iii. that the mutagen will cause an insertion or deletion equally and random
iv. If an insertion, the inserted base will also be random
You’ll want to refer to a codon table for this problem. In addition to online, there is one on page 471.
For example, the odds of getting a UGA stop by an insertion: inserting a U in front of GA somewhere along the gene would be (1 in 2) to get an insertion instead of deletion and; (1 in 4) for getting a U inserted instead of a G, C, or A) and; (1 in 4) for G and (1 in 4) for A in the adjacent positions. This is (0.5)x(0.25)x(0.25)x(0.25): 0.0078 or 0.78% for any one indel event. If we accept this might happen anywhere along the length of the gene, of the 993 indels that might happen, only ~7 would result in a...
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