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(a) Do you expect more null mutations in a gene region with many large introns and a few small exons or a region of the same length with several large exons and only a few small introns? Why? (b) In what parts of an intron and what parts of an exon is a mutation more likely to cause a loss of function?

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Jamar Ferry
Jamar FerryLv2
28 Sep 2019

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Related questions

Based on your success with “fakeprotein” kidney disease, you start looking at other illnesses linked to the FP gene. It turns out that while there are no other human diseases known to be linked to it, there is a disease called Krazy Koala Syndrome and the KKS gene turns out to be very similar to FP in humans. The afflicted Koala’s jump out of trees and attack the much larger animals for no reason, dying very young. When the brains of these Koala;s are evaluated, the have the spongiform character of Mad Cow Disease brains. This is typically caused by aggregates of the protein forming. Like before, there are normal KKS/FP proteins in other tissues. The KKS pre-mRNA looks like this:

Ca2+ bind dimerization Protease

Exon

Intron

Exon

Intron

Exon

The dark blocks are exons and the light blocks are introns. In normal Koala’s, you find only the full length protein (all 3 exons) in most cells, but in neurons you only find the 1st and 2nd exons. In KKS Koala’s you find a mix of the two proteins in neurons, but only the full length everywhere else.

A. There are two possible ways that alternative splicing can result in the formation of these two isoforms. What are they? What does each predict about the mutation that might be responsible for the phenotype?

B. Give an example of an experiment to test for one of these explanations. Describe what result would support the hypothesis.

What are transcription factors? In which groove would you expect them to bind on DNA?

How do the genome, transcriptome and proteome compare in complexity? Which of the following would you expect to be in the exome; introns, exons, 5’ UTRs, 3’ UTRs, promoter sequences?

You are comparing sequences among different species, and you find some sequences are highly conserved. What would you predict would happen if a mutation occurs in a sequence that is highly conserved evolutionarily?

If you discover a highly conserved sequence that is 5’ to the start of transcription, what would you expect mutations in that sequence to do?

a. Reduce fitness

b. Alter gene expression

c. Alter the structure of a protein or proteins

d. All of the above

e. a) and b), but not c)

Question 2. Splicing is complicated. There isconstitutive splicing, and then there is regulated alternativesplicing, and these molecular events can occur in the same ordifferent tissues.

a. What is constitutive splicing?

b. What is alternative splicing?

c. Draw a gene with three exons and twointrons. In this example assume exons 1,2,3 are expressed in onetissue and exons 1,3 are expressed in another. Draw the alternativesplicing, and the resulting RNA from this gene.

d. Draw a model illustrating how sterichindrance can promote alternative splicing with in a gene.

e. An individual is heterozygous, one copy ofthe gene has a mutation in exon 1 and the other copy of the gen ehas a mutation exon 3. Draw their genes, with mutations. What RNAmolecules can be expressed from these alleles? Will thisheterozygote have a mutant or a wild - type phenotype? Explain.Assume the 1/3 variant and the 1/2/3 variant are required indifferent tissues

Question 3 . You haveidentified a 4 exon gene expressed in the nervous system of adiploid animal. Different splice variants are expressed in thenervous tissue at the same time. T he organism under study has agene, unc - 250 , that controls movement and has three differentrecessive mutant alleles: allele s a 1 , a2 , and a3 . All threemutations are nonsens e stop mutations. When a diploid organism ishomozygous for allele a 1 animals die. When homozygous for eitherallele a2 , or allele a3 , animals are very uncoordinated in theirmovement (unc). Alleles a2 and a3 fail to complement allele a1 ,that is to say a1 / a2 and a 1 / a3 heteroallelic animals are veryuncoordinated in their movement (unc). However, a2 / a3 animals arewild type, ie they complement. Using alternative splicingconstruct a logical model for these observations and show whereeach of the mutations would be located in the gene.

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