scholarly journals HYBRID DYSGENESIS IN DROSOPHILA MELANOGASTER: THE BIOLOGY OF FEMALE AND MALE STERILITY

Genetics ◽  
1979 ◽  
Vol 92 (1) ◽  
pp. 161-174
Author(s):  
William R Engels ◽  
Christine R Preston

ABSTRACT High levels of female and male sterility were observed among the hybrids from one of the two reciprocal crosses between a wild strain of D. melanogaster known as π2 and laboratory strains. The sterility, which is part of a common syndrome called hybrid dysgenesis, was found to be associated with the rudimentary condition of one or both of the ovaries or testes. All other tissues, including those of the reproductive system were normal, as were longevity and mating behavior. The morphological details of the sterility closely mimic the agametic condition occurring when germ cells are destroyed by irradiation or by the maternal-effect mutation, grandchildless. We suggest that sterility in hybrid dysgenesis is also caused by failure in the early development of germ cells. There is a thermo-sensitive period beginning at approximately the time of initiation of mitosis among primordial germ cells a few hours before the egg hatches and ending during the early larval stages. Our results suggest that hybrid dysgenesis, which also includes male recombination, mutation and other traits, may be limited to the germ line, and that each of the primordial germ cells develops, or fails to develop, independently of the others. This hypothesis is consistent with the observed frequencies of unilateral and bilateral sterility, with the shape of the thermo-sensitivity curves and with the fact that males are less often sterile than females. The features of this intraspecific hybrid sterility are found to resemble those seen in some interspecific Drosophila hybrids, especially those from the cross D. melanogasfer × D. simulans.

Development ◽  
2022 ◽  
Author(s):  
Yuki Naitou ◽  
Go Nagamatsu ◽  
Nobuhiko Hamazaki ◽  
Kenjiro Shirane ◽  
Masafumi Hayashi ◽  
...  

In mammals, primordial germ cells (PGCs), the origin of the germ line, are specified from the epiblast at the posterior region where gastrulation simultaneously occurs, yet the functional relationship between PGC specification and gastrulation remains unclear. Here, we show that Ovol2, a transcription factor conserved across the animal kingdom, balances these major developmental processes by repressing the epithelial-to-mesenchymal transition (EMT) driving gastrulation and the upregulation of genes associated with PGC specification. Ovol2a, a splice variant encoding a repressor domain, directly regulates EMT-related genes and consequently induces re-acquisition of potential pluripotency during PGC specification, whereas Ovol2b, another splice variant missing the repressor domain, directly upregulates genes associated with PGC specification. Taken together, these results elucidate the molecular mechanism underlying allocation of the germ line among epiblast cells differentiating into somatic cells through gastrulation.


Development ◽  
1981 ◽  
Vol 64 (1) ◽  
pp. 251-258
Author(s):  
Andy McMahon ◽  
Mandy Fosten ◽  
Marilyn Monk

The pattern of expression of the two X chromosomes was investigated in pre-meiotic germ cells from 12½-day-old female embryos heterozygous for the variant electrophoretic forms of the X-linked enzyme phosphoglycerate kinase (PGK-1). If such germ cells carry the preferentially active Searle's translocated X chromosome (Lyon, Searle, Ford & Ohno, 1964), then only the Pgk-1 allele on this chromosome is expressed. This confirms Johnston's evidence (1979,1981) that Pgk-1 expression reflects a single active X chromosome at this time. Extracts of 12½-day germ cells from heterozygous females carrying two normal X chromosomes show both the A and the B forms of PGK; since only one X chromosome in each cell is active, different alleles must be expressed in different cells, suggesting that X-chromosome inactivation is normally random in the germ line. This result makes it unlikely that germ cells are derived from the yolk-sac endoderm where the paternally derived X chromosome is preferentially inactivated. In their pattern of X-chromosome inactivation, germ cells evidently resemble other tissues derived from the epiblast.


Development ◽  
1990 ◽  
Vol 109 (4) ◽  
pp. 911-923 ◽  
Author(s):  
A. Orr-Urtreger ◽  
A. Avivi ◽  
Y. Zimmer ◽  
D. Givol ◽  
Y. Yarden ◽  
...  

Developmental expression of the c-kit proto-oncogene, a receptor tyrosine kinase encoded by the W locus, was investigated by in situ hybridization in normal mouse embryos. Early after implantation transcripts were detectable only in the maternal placenta (6 1/2-7 1/2 days p.c.). Subsequently (8 1/2 days p.c.) numerous ectodermal (neural tube, sensory placodes) and endodermal (embryonic gut) derivatives expressed c-kit. Later transcripts were detected also in the blood islands of the yolk sac and in the embryonic liver, the main sites of embryonic hemopoiesis. Around midgestation, transcripts accumulated in the branchial pouches and also in primordial germ cells of the genital ridges. This complex pattern of expression remained characteristic also later in gestation, when c-kit was expressed in highly differentiated structures of the craniofacial area, in presumptive melanoblasts and in the CNS. In the adult ovary, maternal c-kit transcripts were detected. They were present in the oocytes of both immature and mature ovarian follicles, but not in the male germ line, where c-kit expression may be down regulated. Thus, c-kit activity is complex and appears in multiple tissues including those that also display defects in mutations at the W locus where c-kit is encoded. Correlation between W phenotypes and c-kit expression, as well as the regulation of the complex and multiple expression of polypeptide growth factors and receptors, is discussed.


Development ◽  
1988 ◽  
Vol 102 (3) ◽  
pp. 527-535
Author(s):  
K. Ikenishi ◽  
Y. Tsuzaki

To determine whether the location of ‘germ plasm’-bearing cells [presumptive primordial germ cells (pPGCs)] is crucial for their differentiation into PGCs in Xenopus, [3H]thymidine-labelled pPGCs were implanted into the anterior or posterior halves of the endoderm in unlabelled host neurulae. Labelled PGCs in the genital ridges of experimental tadpoles were investigated by autoradiography. When the labelled pPGCs were implanted into posterior halves of the endoderm where host pPGCs are situated, 65 and 77% of the experimental tadpoles (designated as p-tadpoles) had the labelled PGCs in series I and II, respectively. When implanted into the anterior halves, 20 and 27% of the experimental tadpoles (a- tadpoles) had the labelled PGCs in series I and II, respectively. In p-tadpoles, the average numbers of labelled PGCs per tadpole were 8á7 in series I and 10 in series II, whereas they were 2á0 in a-tadpoles of both series. Both the proportion and the average number in p-tadpoles of both series were significantly different from those in a-tadpoles. In both series, labelled PGCs in p-tadpoles were found to be distributed throughout the genital ridges while those in a-tadpoles were localized only in the anterior part of the ridges. These facts indicate that the location of pPGCs in the endoderm affects their successful migration into the genital ridges, and that not only the presence of the germ plasm but also the proper location in endoderm are prerequisites to PGC differentiation of the germ line cells.


Reproduction ◽  
2013 ◽  
Vol 146 (1) ◽  
pp. R37-R48 ◽  
Author(s):  
Jessica M Stringer ◽  
Sanna Barrand ◽  
Patrick Western

In mice, epiblast cells found both the germ-line and somatic lineages in the developing embryo. These epiblast cells carry epigenetic information from both parents that is required for development and cell function in the fetus and during post-natal life. However, germ cells must establish an epigenetic program that supports totipotency and the configuration of parent-specific epigenetic states in the gametes. To achieve this, the epigenetic information inherited by the primordial germ cells at specification is erased and new epigenetic states are established during development of the male and female germ-lines. Errors in this process can lead to transmission of epimutations through the germ-line, which have the potential to affect development and disease in the parent's progeny. This review discusses epigenetic reprogramming in the germ-line and the transmission of epigenetic information to the following generation.


1978 ◽  
Vol 32 (3) ◽  
pp. 239-247 ◽  
Author(s):  
George Yannopoulos

SUMMARYThe sterility which is associated with male recombination induced by 31.1 MRF was studied genetically and cytologically. In all crosses it was found that female sterility mainly involves failure of the heterozygous females to lay eggs because their ovaries are atrophic. Under the optical microscope, the atrophic ovaries were seen to contain only germaria in their ovarioles. It was also found that in some cases 31.1 MRF affects only one of the two ovaries of the same female. This observation suggests that defective development of atrophic ovaries is not due to influences from the rest of the body but should be attributed to the inability of the germ cells to differentiate. Moreover, various stocks as well as homologous chromosomes were found to react differently to 31.1 MRF with respect to female sterility. In their effect on male sterility it was observed that some strains behave as neutral and others as reactive when mated with 31.1/Cy L4 males.


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