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How many proteins can be produced from a gene with 4 exons and 3introns via alternative splicing (not including alternative 5' and3' splice sites)? Exons 1 and 4 are constitutive exons and exons 2and 3 can be alternatively spliced.

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Bunny Greenfelder
Bunny GreenfelderLv2
29 Sep 2019
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Related questions

You obtain the sequence of a gene containing 10 exons, 9 introns, and a 3' UTR containing a polyadenylation consensus sequence. The fifth intron also contains a polyadenylation site. To test whether both polyadenylation sites are used, you isolate mRNA and find a longer transcript from muscle tissue and a shorter transcript from all other tissues. Which of the following is the most likely mechanism underlying these alternative transcripts?

A. The mRNA in muscle cells is edited to eliminate the polyadenylation sequence in exon 5

B. An alternative CPSF protein is expressed in muscle cells with lower affinity for the polyadenylation sequence in exon 5.

C. The fifth exon is spliced out of the mature mRNA transcript in muscle cells

D. Muscle cells have less effective polyadenylation than other tissues

You obtain the sequence of a gene containing 10 exons, 9 introns, and a 3′ UTR containing a polyadenylation consensus sequence. The fifth exon also contains a polyadenylation site. To test whether both polyadenylation sites are used, you isolate mRNA and find a longer transcript from muscle tissue and a shorter transcript from all other tissues. Which of the following is the most likely mechanism underlying these alternative transcripts?

A) The fifth exon is spliced out of the mature mRNA transcript in muscle cells.

B) Muscle cells have less effective polyadenylation than other tissues.

C) An alternative CPSF protein is expressed in muscle cells with lower affinity for the polyadenylation sequence in exon 5.

D) The mRNA in muscle cells is edited to eliminate the polyadenylation sequence in exon 5

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.

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