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|Title:||A Study of Primordial Germ Cell Migration and Gonadogenesis in Normal and Sterile Steel Mutant Mice|
|Authors:||McCoshen, Adrian John|
|Department:||Medical Sciences (Growth and Development)|
|Keywords:||Medical Sciences;Medical Sciences|
|Abstract:||<p>The development of murine gonads commences in both males and females as indifferent appearing blastemata around the 10th day of embryogenesis. Within the following two days, the, gonadal blastemata became heavily populated with the primordial germ cells which migrate in from extragonadal sites.</p> <p>The process of gonadal sex differentiation is first evident in males where the appearance of sex cords marks testicular histogenesis. Ovarian development is largely marked by the fact that female gonads do not resemble testes and also by the early transformation of oogonia into oocytes.</p> <p>It has been proposed by a number of investigators that the absence of the primordial germ cells in the gonadal blastemata during the indifferent stage of gonadogenesis would result in the failure of sex cord differentiation to take place within the gonadal soma. Other investigators have proposed that gonadal sex differentiation is not dependent upon the presence of germ cells within the gonadal soma.</p> <p>To resolve this controversy mice carrying the alleles Steel/Steel Dickie (S1/S1ᵈ) were selected since the Steel mutation is known to severely affect the primordial germ cell line prior to its populating the gonadal ridges before sex cord differentiation. The experiment therefore is a natural one not requiring chemical or physical ablation of the germ cell line at the time it is first histochemically identifiable in sites far removed from the gonadal anlages.</p> <p>Primordial germ cells were identified histochemically by an azo dye technique in 27 day 9, 33 day 10, 33 day 11 and 21 day 12 embryos which were obtained from matings between mature WC/ReJ-S1/+ females and C57B1/6J-S1ᵈ/+ males. One fourth of the embryo zygous S1/S1ᵈ mutation. Failure to the germ cell population to increase after 9 days gestation occurred in 26% of the embryos. These embryos were classified as the mutant S1/S1ᵈ group. The primordial germ cells of the mutants, though few in number, were found to follow a normal migratory pattern to the gonadal ridges. Gonadogenesis was studied in 227 fetuses of 12-18 days gestation and in animals from birth to maturity. The genetic sex of fetuses was determined by the presence or absence of sex chromatin in amnion cells. Prior to day 14, genotypes were established as normal or mutant according to the germ cell population present in one gonad from each fetus. After day 14 the genotypes were determined from red blood cell samples, the S1/S1ᵈ fetuses displaying the macrocytic anemia characteristic of this mutation.</p> <p>The ratio of mutant males to mutant females was the normal 1:1, and the number of mutants identified was within the expected 25% frequency. Despite a paucity of germ cells, mutant gonads differentiated according to their genetic sex. Although mutant gonads are composed almost entirely of somatic tissue they grow at the same rate as the somatic component of normal gonads up to day 16 post coitus in males, and to the day of birth in females. The overall pattern of growth was similar to that seen in normals. The Mullerian and Wolffian ducts as well as the external genitalia also developed according to gonadal sex in the mutants.</p> <p>In those mutant gonads which contained few germ cells, they grew and differentiated in the same manner as did those of the normals up to birth. By maturity, no mutant germ cells were found to have differentiated beyond prophase of meiosis I.</p> <p>It is concluded that sexual differentiation and gonadogenesis can take place in the absence or at least in the near absence of germ cells. The Steel mutation appears to act in preventing the proliferation of the primordial germ cells and their capacity to complete meiosis I of gametogenesis. The mutation, however, does not affect the evolution of the germ cells from their source nor the capacity of the germ cells to migrate to the gonadal blastemata.</p>|
|Appears in Collections:||Open Access Dissertations and Theses|
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