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When cows have twin calves of unlike sex (fraternal twins), the female twin is usually sterile and has masculinized reproductive organs. This calf is referred to as a freemartin. In cows, twins may share a common placenta and thus fetal circulation. Predict why a freemartin develops.

Short Answer

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Question: Explain the process of freemartin development in twin calves of different sexes. Answer: Freemartin development occurs in female calves born twin to a male calf due to hormonal interference caused by shared placenta and fetal circulation. The male twin produces testosterone and anti-Müllerian hormone (AMH), which can be transferred to the female twin. Testosterone leads to the masculinization of her reproductive organs, and AMH inhibits the development of female reproductive structures. This results in the female twin becoming a freemartin, having masculinized reproductive organs and being sterile.

Step by step solution

01

Understand what a freemartin is

A freemartin is a female calf born twin to a male calf. Due to shared placenta and fetal circulation, the female twin experiences hormonal interference, masculinizing her reproductive organs and leading to sterility.
02

Identify the hormones involved in sexual differentiation

Two hormones play a pivotal role in sexual differentiation: testosterone and anti-Müllerian hormone (AMH). Testosterone is responsible for the development of male genitalia, while AMH prevents the formation of female reproductive structures.
03

Understand the role of shared placenta and fetal circulation

In cows, twins may share a common placenta and thus fetal circulation. This enables substances, such as hormones, to be transferred between the two fetuses. In the case of twin calves of unlike sex, the hormones from the male twin can interfere with the female twin's sexual differentiation process.
04

Explain how hormonal interference leads to freemartin development

The male twin produces testosterone and AMH during its development. These hormones can be transferred to the female twin due to shared fetal circulation. The presence of testosterone in the female twin can cause the masculinization of her reproductive organs, while the AMH can inhibit the development of her female reproductive structures. As a result, the female twin becomes a freemartin, having masculinized reproductive organs and being sterile.
05

Summarize the prediction

A freemartin develops due to the hormonal interference caused by the shared placenta and fetal circulation. The male twin's hormones, testosterone and AMH, impact the female twin's sexual differentiation process, leading to the masculinization of her reproductive organs and inhibition of the development of female reproductive structures, ultimately resulting in sterility.

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Key Concepts

These are the key concepts you need to understand to accurately answer the question.

Fraternal Twins
Fraternal twins are often seen in mammals, including cows, and occur when two different eggs are fertilized by two separate sperm. Unlike identical twins, who come from the same egg and therefore share identical genetic material, fraternal twins are genetically unique from one another. In bovines, this means that the siblings can be of different sexes, which sets the stage for intriguing biological interactions.
  • They develop from two distinct fertilized eggs.
  • Each twin can be a different sex and have different genetic characteristics.
  • Unlike identical twins, they do not share the same amniotic sac.
In the case of a female calf born fraternal twin to a male calf, she faces a unique challenge. Due to a phenomenon called "freemartinism," her reproductive system can be heavily influenced by her brother. This results in a small, but significant phenomenon in cattle where the female twin is often sterile due to hormonal influences shared with her male twin.
Hormonal Interference
Hormonal interference plays a crucial role in the development of freemartins. When twin calves share a placenta, the possibility of hormonal cross-talk arises. This generally involves the male hormones influencing the development of the female twin.
The key hormonal players in this interference include:
  • Testosterone: Produced by the male fetus, it is essential for the development of male genitalia, but when transferred to the female twin, it can cause masculinization of her reproductive organs.
  • Anti-Müllerian Hormone (AMH): Normally prevents the formation of female reproductive structures in males; when present in females, it also hinders proper sexual differentiation.
The transfer of these hormones, primarily testosterone and AMH, from the male to the female twin through shared fetal circulation results in a disruption of the typical development process, turning the female twin into a freemartin.
Sexual Differentiation
Sexual differentiation is an intricate process determined largely by hormones and genetic factors. In a typical scenario, the presence of the male Y chromosome leads to the production of male-specific hormones like testosterone and AMH, guiding the embryo towards male development.
However, when these hormones are present in a developing female fetus (due to shared fetal circulation), they can override the genetic instructions intended for female sexual differentiation.
  • Inhibited development of female reproductive structures due to AMH.
  • Masculinization of certain female reproductive organs due to testosterone.
This imbalance between genetics and hormonal influences during gestation is primarily why a female calf can develop masculine characteristics when she has a male twin, resulting in the condition known as freemartinism.
Shared Placenta
A shared placenta is a vital, though unusual aspect of the twin pregnancy in cows that can lead to freemartinism. In cattle, occasionally the placenta is a single connecting structure between the mother and both fetuses, creating a shared blood supply and nutrient distribution system.
  • It allows for the mixing of hormones between the fetuses.
This shared circulation is the main avenue through which male hormones like testosterone and AMH reach the female twin.
The shared placenta creates an environment where these hormonal influences can skew the development of the female fetus towards masculinity, resulting in the condition where the female calf becomes a freemartin, typically showing sterility and varying degrees of male characteristics in her reproductive system. Hence, the placental sharing indirectly determines physiological outcomes by facilitating hormone travel between the twins.

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Most popular questions from this chapter

Review the Chapter Concepts list on p. \(83 .\) These all center on sex determination or the expression of genes encoded on sex chromosomes. Write a short essay that discusses sex chromosomes as they contrast with autosomes.

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?

Indicate the expected number of Barr bodies in interphase cells of individuals with (a) triple \(X\) syndrome \((X X X)\) (b) \(\mathrm{XYY}\) syndrome, (c) Klinefelter syndrome, (d) Turner syndrome, and karyotype \(48, \mathrm{XXXX}\)

The genes encoding the red-and green-color-detecting proteins of the human eye are located next to one another on the X chromosome and probably evolved from a common ancestral pigment gene. The two proteins demonstrate 76 percent homology in their amino acid sequences. A normal-visioned woman with both genes on each of her two X chromosomes has a redcolor-blind son who was shown to have one copy of the greendetecting gene and no copies of the red-detecting gene. Devise an explanation for these observations at the chromosomal level (involving meiosis).

In this chapter, we have 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, 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?

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