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Chapter 5: Problem 9

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

Short Answer

Expert verified
Answer: Nondisjunction in human female gametes can result in offspring with Klinefelter syndrome (XXY) or Turner syndrome (X0), due to an abnormal number of sex chromosomes in the zygote. Klinefelter syndrome, which affects males, presents symptoms such as reduced fertility and small testicles, while Turner syndrome affects females with features like short stature and infertility.

Step by step solution

01

Understanding nondisjunction

Nondisjunction is an error in meiosis, the process that creates gametes (egg and sperm cells). During meiosis, the chromosomes should separate properly, resulting in gametes with the right number of chromosomes. However, in nondisjunction, chromosomes fail to separate correctly, producing gametes with an abnormal number of chromosomes. In this exercise, we'll focus on nondisjunction in human female gametes (egg cells).
02

Normal chromosome distribution

In humans, each cell contains 46 chromosomes in 23 pairs. One chromosome of each pair is inherited from the mother, and the other from the father. Sex chromosomes determine an individual's sex: females have two X chromosomes (XX), while males have one X and one Y chromosome (XY). During normal meiosis in females, each egg cell should receive one X chromosome.
03

Nondisjunction in human female gametes

In the case of nondisjunction, an error occurs during meiosis in the egg cell formation. The X chromosomes fail to separate properly, leading to egg cells with either two X chromosomes or no X chromosome instead of just one.
04

Fertilization with normal male gamete

A normal male gamete contains either an X or a Y chromosome. When a male gamete (sperm) with an X chromosome fertilizes an egg cell with two X chromosomes (due to nondisjunction), the resulting zygote will have three sex chromosomes (XXY). This condition is known as Klinefelter syndrome. On the other hand, if a male gamete with a Y chromosome fertilizes an egg cell without an X chromosome (also due to nondisjunction), the resulting zygote will have only one sex chromosome (X0). This condition is called Turner syndrome.
05

Klinefelter syndrome and Turner syndrome offspring

The offspring resulting from the aforementioned cases of nondisjunction will have the Klinefelter or Turner syndrome. Klinefelter syndrome (XXY) affects males, causing symptoms like reduced fertility, small testicles, and enlarged breast tissue. Turner syndrome (X0) affects females and is characterized by short stature, infertility, and heart defects, among other features. In summary, nondisjunction in human female gametes can give rise to Klinefelter and Turner syndrome offspring when these abnormal egg cells are fertilized by a normal male gamete. This is because the chromosomes fail to separate properly during meiosis, which leads to zygotes with an unusual number of sex chromosomes.

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Most popular questions from this chapter

What specific observations (evidence) support the conclusions about sex determination in Drosophila and humans?

In this chapter, we have focused on sex differentiation, sex chro- mosomes, 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, you should answer the following fundamental questions: (a) How do we know that in humans the X chromosomes play no role in sex determination, while the Y chromosome causes maleness and its absence causes femaleness? (b) How did we originally (in the late 1940 s) analyze the sex ratio at conception in humans, and how has our approach to studying this issue changed in \(2015 ?\) (c) 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? (d) 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?

In mice, the X-linked dominant mutation Testicular feminization (Tfm) eliminates the normal response to the testicular hormone testosterone during sexual differentiation. An XY mouse bearing the \(T f m\) allele on the \(X\) chromosome develops testes, but no further male differentiation occurs-the external genitalia of such an animal are female. From this information, what might you conclude about the role of the Tfm gene product and the \(\mathrm{X}\) and \(\mathrm{Y}\) chromosomes in sex determination and sexual differen- tiation in mammals? Can you devise an experiment, assuming you can "genetically engineer" the chromosomes of mice, to test and confirm your explanation?

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?

Distinguish between (a) the concepts of sexual differentiation and sex determination and (b) Protenor and Lygaeus modes of sex determination.
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