This one has stumped me for quite a while... 5. Assume that defects in a hypothe

Question

This one has stumped me for quite a while...

5. Assume that defects in a hypothetical gene, X, have been linked to antisocial behavior. Two copies of a defective gene X predispose a child to bad behavior from childhood, while a single copy of the gene seems to produce no symptoms until adulthood. Since the effects of the gene can be counteracted if treatment is started early enough, a program of voluntary genetic testing is being carried out with delinquent prospective parents. Charles S. and Caril Ann F. have been arrested on charges of robbery and assault, and Caril Ann is pregnant with Charles’s child. You obtain DNA samples from Charles, Caril Ann, and the fetus. You digest these samples with Not I and use these samples to perform two Southern Blots, which you probe with two different oligonucleotide probes, A and B, that hybridize to different parts of the normal gene X, as shown in Figure 10-3A. Your results are shown in Figure 10-3B.

Explanation / Answer

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After some thoughts, here's one solution.

A. All three people have some defect, but for different reason! Both parents carry a different defective copy of the gene (in addition to a w.t. copy) and thus they are both predisposed to delinquency. Poor child... he has mutations on both alleles of this gene and thus he'll have bad behavior. Could be a boy, or a girl,.. who knows.

B. Both parents have a single, different defect. The child has two different, defective copies of the gene.

C. Charles has one w.t. allele. This explains the higher size band on both panels. He also has a mutant allele (not deletion) that both disrupts recognition of probe A AND creates a new Not I site there. This explains the absence of a second band on the left panel - because the mutant disrupted the recognition of probe A - and the small size with probe B where the mutation doesn't affect probe B recognition. That mutant allele is carried over to the child where it is not recognized by probe A, but it is recognized by probe B as low size.

Caril Ann has a similar genotype but a little different:

She has one w.t. allele that is explained by the higher size band on both panels. She also has a mutant allele (not deletion) that both disrupts recognition of probe B AND creates a new Not I site there. This explains the absence of a second band on the right panel - because the mutant disrupted the recognition of probe B - and the small size with probe A where the mutation doesn't affect probe A recognition. That mutant allele is carried over to the child where it is not recognized by probe B, but it is recognized by probe A as low size.

Hopefully there is a simpler explanation than the above.

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