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With reference to sex determination in humans, discuss: i) X chromosome
inactivation; and ii) Testicular feminization
Step by step
Solved in 2 steps
- Discuss whether the following individuals (1) have male or female gonads, (2) are phenotypically male or female (Wolffian or Muellerian ducts. External genitalia) and (3) are sterile or fertile. a) XY, homozygous for a recessive mutation in the testosterone biosynthetic pathway, producing no testosterone b) XX, heterozygous for a dominant mutation in the testosterone biosynthetic pathway, which causes continuous production of testosteroneWith relevance to sex determination in humans, discuss: i) X chromosome inactivation; and ii) Testicular feminization Provide detail examples.a) Define Disorders of Sex Development (DSD). b) Explain why gene mutations affecting gonad development may lead to DSD conditions. c) What is sex-chromosome mosaicism? When and how may this mosaicism arise?
- 1) A variety of abnormalities in the numbers of sex chromosomes exist because of nondisjunction during gametogenesis. Discuss the signs and problems associated with conditions such as Klinefelter and Turner syndromes.Which of the following is TRUE about the mechanism of sex determination? A) The product of the SRY gene converts the bipotential gonads into testes. B) The development of an ovary is conditioned by the presence of two X chromosomes. (C) Testosterone promotes the degeneration of the Mullerian duct. D. The ovary produces a Wolffian inhibition factor that causes the Wolffian duct to degenerate. E) The "feminization" of accessory sex orgarts is promoted by the ovary.Give the chromosomal constitution & related sex in each of the following :-i) Turner syndromeii) Klinefilter syndrome
- Select the FALSE statement/s: A) The functional layer of the endometrium sloughs off when estrogen levels are at their lowest but progesterone levels at their highest. 1 OB) Every month, the 20 secondary follicles release 20 ova. OC) XX genotypic female exposed to high levels of androgen in utero will develop male-like exfernal genitalia OD) Both A and B OE) Both B and CDiscuss whether the following individuals (1) have male or female gonads, (2) are phenotypically male or female (Wolffian or Muellerian ducts. External genitalia) and (3) are sterile or fertile.Which of the following statements are false? A) An oocyte completes meiosis after a sperm penetrates it. B) The earliest stages of spermatogenesis occur closest to the lumen of the seminiferous tubules. C) Fertilization occurs in the oviduct. D) Effective hormonal contraceptives are currently available only for females. E) Spermatogenesis and oogenesis require different temperatures. F) Fragmentation is a type of asexual reproduction wherein an organism produces gemmules which are collections of many cells surrounded by a body wall. G) Lobsters and insects can reproduce via fragmentation.
- Why is a genetic predisposition suggested for testicular cancer?Which of the following statements accurately describes the pathogenesis of polycystic ovarian syndrome? Question 28 options: a) Excessive androgens that affect follicular decline by suppressing apoptosis, enabling follicles, which normally disintegrate to survive b) A decrease in leptin levels that reduces the hypothalamic pulsatility of GnRH, which reduces the number of follicles that mature c) A disorder of the anterior pituitary that increases the release of FSH, which reduces the release of LH d) Testosterone that stimulates androgen secretion by the ovarian stroma and reduces SHBG indirectly_____ is a form of 46,XY intersex that affects chromosomal males. It is by far the most common form of 46,XY intersex. These individuals have testes that produce testosterone, but their bodies lack working androgen receptors. When these individuals are born they often have female-typical genitalia, and they develop female secondary sex characteristics at puberty. They also tend to develop a female gender identity. A) Androgen insensitivity syndrome B) Turner's syndrome C)Congenital adrenal hyperplasia D) 5-alpha reductase deficiency