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Can the Lyon hypothesis be tested in a human female who is homozygous for one allele of the X-linked G6PD gene? Why, or why not?

Short Answer

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Why or why not? Answer: No, the Lyon hypothesis cannot be tested in a human female who is homozygous for one allele of the X-linked G6PD gene. This is because both X chromosomes carry the same gene copy, so even if X-inactivation occurs, it would not lead to any observable differences in gene expression in this specific situation.

Step by step solution

01

Understanding X-inactivation (Lyon hypothesis)

X-inactivation is a process in which one of the two X chromosomes in female mammals is randomly inactivated to achieve gene dosage compensation. This is important because males only have one X chromosome, so if females expressed genes from both of their X chromosomes, they could end up with twice the amount of X-linked gene product, which might lead to an imbalance between different gene products. The Lyon hypothesis proposes that this random X-inactivation occurs early in development, and the inactivated X chromosome forms a compact structure called a Barr body.
02

Knowing the role of G6PD gene

The G6PD gene is an X-linked gene that encodes an enzyme called glucose-6-phosphate dehydrogenase, which plays an essential role in red blood cell metabolism. Homozygous refers to a situation when an organism possesses two identical copies of a particular allele. So a female Homo sapiens who is homozygous for one allele of the X-linked G6PD gene would have the same G6PD gene variant on both of her X chromosomes.
03

Testing the Lyon hypothesis in a G6PD homozygous female human

To investigate Lyon hypothesis, it is necessary to examine whether both X chromosomes are active or if one of them is inactivated, leading to a gene dosage balance. In a female human who is heterozygous for the X-linked G6PD gene (carrying two different alleles), cell populations would express different alleles due to random X-inactivation, making it possible to test the Lyon hypothesis. However, in a female human who is homozygous for one allele of the X-linked G6PD gene, there would be no difference in gene expression between the cells where the first X chromosome is inactivated and those where the second X chromosome is inactivated. Both copies of the gene are the same, so even if X-inactivation occurs, it would not lead to any observable differences in gene expression, making it impossible to test Lyon hypothesis in such cases. In summary, the Lyon hypothesis cannot be tested in a human female who is homozygous for one allele of the X-linked G6PD gene because both X chromosomes carry the same gene copy, so X-inactivation will not lead to any observable differences in gene expression in this specific situation.

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Most popular questions from this chapter

In this chapter, we focused on sex differentiation, sex chromosomes, and genetic mechanisms involved in sex determination. At the same time, we found many opportunities to consider the methods and reasoning by which much of this information was acquired. From the explanations given in the chapter, what answers would you propose to the following fundamental questions? (a) How do we know that specific genes in maize play a role in sexual differentiation? (b) How do we know whether or not a heteromorphic chromosome such as the Y chromosome plays a crucial role in the determination of sex? (c) How do we know that in humans the X chromosomes play no role in human sex determination, while the Y chromosome causes maleness and its absence causes femaleness? (d) How did we learn that, although the sex ratio at birth in humans favors males slightly, the sex ratio at conception favors them much more? (e) How do we know that Drosophila utilizes a different sexdetermination mechanism than mammals, even though it has the same sex-chromosome compositions in males and females? (f) How do we know that X chromosomal inactivation of either the paternal or maternal homolog is a random event during early development in mammalian females?

What type of evidence supports the conclusion that the primary sex ratio in humans is much higher than the secondary sex ratio?

Describe how nondisjunction in human female gametes can give rise to Klinefelter and Turner syndrome offspring following fertilization by a normal male gamete.

Distinguish between the concepts of sexual differentiation and sex determination.

In a number of organisms, including Drosophila and butterflies, genes that alter the sex ratio have been described. In the pest species Musca domesticus (the house fly), Aedes aegypti (the mosquito that is the vector for yellow fever), and Culex pipiens (the mosquito vector for filariasis and some viral dis- eases), scientists are especially interested in such genes. Sex in Culex is determined by a single gene pair, \(M m\) being male and \(m m\) being female. Males homozygous for the recessive gene \(d d\) never produce many female offspring. The \(d d\) combination in males causes fragmentation of the \(m\) -bearing dyad during the first meiotic division, hence its failure to complete spermatogenesis. (a) Account for this sex-ratio distortion by drawing labeled chromosome arrangements in primary and secondary spermatocytes for each of the following genotypes: \(M m D d\) and \(M m d d .\) How do meiotic products differ between \(D d\) and \(d d\) genotypes? Note that the diploid chromosome number is 6 in Culex pipiens and both \(D\) and \(M\) loci are linked on the same chromosome. (b) How might a sex-ratio distorter such as \(d d\) be used to control pest population numbers?

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