Expression of the Sex-lethal gene is controlled at multiple levels during Drosophila oogenesis

Development ◽  
1993 ◽  
Vol 118 (3) ◽  
pp. 797-812 ◽  
Author(s):  
D. Bopp ◽  
J.I. Horabin ◽  
R.A. Lersch ◽  
T.W. Cline ◽  
P. Schedl
Keyword(s):  
Germ Cells ◽  
Germ Line ◽  
Basic Mechanism ◽  
Lethal Gene ◽  
Protein Distribution ◽  
Wild Type ◽  
Protein Levels ◽  
Germ Cell Differentiation ◽  
Cytoplasmic Accumulation ◽  
Sex Lethal

In addition to controlling somatic sexual development in Drosophila melanogaster, the Sex-lethal (Sxl) gene is required for proper differentiation of female germ cells. To investigate its role in germ-line development, we have examined the expression of Sxl in wild-type ovaries and ovaries that are defective in early steps of germ cell differentiation. As in the soma, the basic mechanism for on/off regulation of Sxl relies on sex-specific processing of its transcripts in germ cells. One class of female-sterile mutations, which includes fs(1)1621 and the tumorous-ovary-producing allele of the ovarian tumor gene, otu1, is defective in the splicing process. These mutants have germ lines with high amounts of Sxl RNA spliced in the male mode and a severe reduction of protein levels in the germ cells. Another class of female-sterile mutations produces a phenotype similar to that seen in fs(1)1621 and otu1 but appears to express normal levels of Sxl protein in the germ cells. However, this second class does not show the changes in protein distribution normally observed in wild-type germ cells. In the wild-type germarium, the non-differentiated germ cells show a strong cytoplasmic accumulation of Sxl protein followed, as the germ cells differentiate, by a dramatic reduction and redistribution of the protein into nuclear foci. Interestingly, two female-sterile alleles of Sxl, Sxlf4 and Sxlf5 belong to the second class, which shows persistent cytoplasmic accumulation of Sxl protein. These Sxl female-sterile mutants encode an altered protein indicating that Sxl regulates processes that eventually lead to the changes in Sxl protein distribution. Lastly, we demonstrate that during the final stages of oogenesis several mechanisms must operate to prevent the progeny from inheriting Sxl protein. Conceivably, this regulation safeguards the inadvertent activation of the Sxl autoregulatory feedback loop in the male zygote.

Sex determination in the germ line of Drosophila melanogaster: activation of the gene Sex-lethal

Development ◽  
1993 ◽  
Vol 118 (3) ◽  
pp. 813-816 ◽  
Author(s):  
B. Granadino ◽  
P. Santamaria ◽  
L. Sanchez
Keyword(s):  
Drosophila Melanogaster ◽  
Germ Cells ◽  
Germ Line ◽  
Wild Type ◽  
Female Development ◽  
Pole Cell ◽  
Somatic Tissues ◽  
Wild Type Female ◽  
Sex Lethal ◽  
Pole Cell Transplantation

The germ line exhibits sexual dimorphism as do the somatic tissues. Cells with the 2X;2A chromosome constitution will follow the oogenic pathway and X;2A cells will develop into sperm. In both somatic and germ-line tissues, the sexual pathway chosen by the cells depends on the gene Sex-lethal (Sxl), whose function is continuously needed for female development. In the soma, the sex of the cells is autonomously determined by the X:A signal while, in the germ line, the sex is determined by cell autonomous (the X:A signal) and somatic inductive signals. Three X-linked genes have been identified, scute (sc), sisterless-a (sis-a) and runt (run), that determine the initial functional state of Sxl in the soma. Using pole cell transplantation, we have tested whether these genes are also needed to activate Sxl in the germ line. We found that germ cells simultaneously heterozygous for sc, sis-a, run and a deficiency for Sxl transplanted into wild-type female hosts develop into functional oocytes. We conclude that the genes sc, sis-a and run needed to activate Sxl in the soma seem not to be required to activate this gene in the germ line; therefore, the X:A signal would be made up by different genes in somatic and germ-line tissues. The Sxlf7M1/Sxlfc females do not have developed ovaries. We have shown that germ cells of this genotype transplanted into wild-type female hosts produce functional oocytes. We conclude that the somatic component of the gonads in Sxlf7M1/Sxlfc females is affected, and consequently germ cells do not develop.(ABSTRACT TRUNCATED AT 250 WORDS)

Genetic evidence that the sans fille locus is involved in Drosophila sex determination.

Genetics ◽  
1988 ◽  
Vol 120 (1) ◽  
pp. 159-171
Author(s):  
B Oliver ◽  
N Perrimon ◽  
A P Mahowald
Keyword(s):  
Sex Determination ◽  
Dosage Compensation ◽  
Germ Line ◽  
Ovarian Tumors ◽  
Lethal Gene ◽  
Nurse Cells ◽  
Loss Of Function ◽  
Wild Type ◽  
Sex Lethal

Abstract Females homozygous for sans fille1621 (= fs(1)1621) have an abnormal germ line. Instead of producing eggs, the germ-line cells proliferate forming ovarian tumors or excessive numbers of nurse cells. The Sex-lethal gene product(s) regulate the branch point of the dosage compensation and sex determination pathways in the soma. The role of Sex-lethal in the germ line is not clear but the germ line of females homozygous for female sterile Sex-lethal alleles or germ-line clones of loss-of-function alleles are characterized by ovarian tumors. Females heterozygous for sans fille1621 or Sex-lethal are phenotypically wild type with respect to viability and fertility but females trans-heterozygous for sans fille1621 and Sex-lethal show ovarian tumors, somatic sexual transformations, and greatly reduced viability.

scholarly journals Sex determination in Drosophila: sis-b, a major numerator element of the X:A ratio in the soma, does not contribute to the X:A ratio in the germ line

Development ◽  
1993 ◽  
Vol 117 (2) ◽  
pp. 763-767 ◽  
Author(s):  
M. Steinmann-Zwicky
Keyword(s):  
Sex Determination ◽  
Germ Cells ◽  
Germ Line ◽  
Somatic Cells ◽  
Present Evidence ◽  
Primary Signal ◽  
Sex Lethal

In soma and germ cells of Drosophila, the X:A ratio builds a primary signal for sex determination, and in both tissues Sex-lethal (Sxl) function is required for cells to enter the female pathway. In somatic cells of XX animals, the products of X-chromosomal elements of the X:A ratio activate Sxl. Here I show that sisterless-b (sis-b), which is the X-chromosomal element of the somatic X:A ratio that has best been analysed, is not required for oogenesis. I also present evidence that Sxl function might not be sufficient to direct germ cells into the female pathway. These results show that the elements forming the X:A ratio in the germ line are different from the elements forming the X:A ratio in the soma and they suggest that, in the germ line, Sxl might not be regulated by the X:A ratio.

scholarly journals The mog-1 gene is required for the switch from spermatogenesis to oogenesis in Caenorhabditis elegans.

Genetics ◽  
1993 ◽  
Vol 133 (4) ◽  
pp. 919-931 ◽  
Author(s):  
P L Graham ◽  
J Kimble
Keyword(s):  
Caenorhabditis Elegans ◽  
Sex Determination ◽  
Germ Cells ◽  
Germ Line ◽  
Loss Of Function ◽  
Wild Type ◽  
Per Se ◽  
Post Transcriptional Regulation ◽  
Germline Sex Determination ◽  
Embryonic Death

Abstract Caenorhabditis elegans hermaphrodites make first sperm, then oocytes. By contrast, animals homozygous for any of six loss-of-function mutations in the gene mog-1 (for masculinization of the germ line) make sperm continuously and do not switch into oogenesis. Therefore, in mog-1 mutants, germ cells that normally would become oocytes are transformed into sperm. By contrast, somatic sexual fates are normal, suggesting that mog-1 plays a germ line-specific role in sex determination. Analyses of double mutants suggest that mog-1 negatively regulates the fem genes and/or fog-1: mog-1; fem and mog-1; fog-1 double mutants all make oocytes rather than sperm. Therefore, we propose that wild-type mog-1 is required in the hermaphrodite germ line for regulation of the switch from spermatogenesis to oogenesis rather than for specification of oogenesis per se. In addition to its role in germline sex determination, maternal mog-1 is required for embryogenesis: most progeny of a mog-1; fem or mog-1; fog-1 mother die as embryos. How might the roles of mog-1 in the sperm/oocyte switch and embryogenesis be linked? Previous work showed that fem-3 is regulated post-transcriptionally to achieve the sperm/oocyte switch. We speculate that mog-1 may function in the post-transcriptional regulation of numerous germ-line RNAs, including fem-3. A loss of mog-1 might inappropriately activate fem-3 and thereby abolish the sperm/oocyte switch; its loss might also lead to misregulation of maternal RNAs and thus embryonic death.

Transformation of the germ line into muscle in mes-1 mutant embryos of C. elegans

Development ◽  
1995 ◽  
Vol 121 (9) ◽  
pp. 2961-2972 ◽  
Author(s):  
S. Strome ◽  
P. Martin ◽  
E. Schierenberg ◽  
J. Paulsen
Keyword(s):  
Cell Fate ◽  
Germ Cells ◽  
Germ Line ◽  
Primordial Germ Cells ◽  
Primordial Germ Cell ◽  
Wild Type ◽  
C Elegans ◽  
Stem Cell Divisions ◽  
Asymmetric Partitioning

Mutations in the maternal-effect sterile gene mes-1 cause the offspring of homozygous mutant mothers to develop into sterile adults. Lineage analysis revealed that mutant offspring are sterile because they fail to form primordial germ cells during embryogenesis. In wild-type embryos, the primordial germ cell P4 is generated via a series of four unequal stem-cell divisions of the zygote. mes-1 embryos display a premature and progressive loss of polarity in these divisions: P0 and P1 undergo apparently normal unequal divisions and cytoplasmic partitioning, but P2 (in some embryos) and P3 (in most embryos) display defects in cleavage asymmetry and fail to partition lineage-specific components to only one daughter cell. As an apparent consequence of these defects, P4 is transformed into a muscle precursor, like its somatic sister cell D, and generates up to 20 body muscle cells instead of germ cells. Our results show that the wild-type mes-1 gene participates in promoting unequal germ-line divisions and asymmetric partitioning events and thus the determination of cell fate in early C. elegans embryos.

Germ cell differentiation and proliferation in the developing testis of the South American plains viscacha, Lagostomus maximus (Mammalia, Rodentia)

Zygote ◽  
2011 ◽  
Vol 20 (3) ◽  
pp. 219-227 ◽  
Author(s):  
C.R. Gonzalez ◽  
M.L. Muscarsel Isla ◽  
N.A. Fraunhoffer ◽  
N.P. Leopardo ◽  
A.D. Vitullo
Keyword(s):  
Germ Cell ◽  
Germ Cells ◽  
Germ Line ◽  
Late Gestation ◽  
Nuclear Antigen ◽  
South American ◽  
The South ◽  
Pluripotency Marker ◽  
Germ Cell Differentiation ◽  
Lagostomus Maximus

SummaryCell proliferation and cell death are essential processes in the physiology of the developing testis that strongly influence the normal adult spermatogenesis. We analysed in this study the morphometry, the expression of the proliferation cell nuclear antigen (PCNA), cell pluripotency marker OCT-4, germ cell marker VASA and apoptosis in the developing testes of Lagostomus maximus, a rodent in which female germ line develops through abolished apoptosis and unrestricted proliferation. Morphometry revealed an increment in the size of the seminiferous cords with increasing developmental age, arising from a significant increase of PCNA-positive germ cells and a stable proportion of PCNA-positive Sertoli cells. VASA showed a widespread cytoplasmic distribution in a great proportion of proliferating gonocytes that increased significantly at late development. In the somatic compartment, Leydig cells increased at mid-development, whereas peritubular cells showed a stable rate of proliferation. In contrast to other mammals, OCT-4 positive gonocytes increased throughout development reaching 90% of germ cells in late-developing testis, associated with a conspicuous increase in circulating FSH from mid- to late-gestation. TUNEL analysis was remarkable negative, and only a few positive cells were detected in the somatic compartment. These results show that the South American plains viscacha displays a distinctive pattern of testis development characterized by a sustained proliferation of germ cells throughout development, with no signs of apoptosis cell demise, in a peculiar endocrine in utero ambiance that seems to promote the increase of spermatogonial number as a primary direct effect of FSH.

scholarly journals Genetic evidence that the ovo locus is involved in Drosophila germ line sex determination.

Genetics ◽  
1990 ◽  
Vol 125 (3) ◽  
pp. 535-550 ◽  
Author(s):  
B Oliver ◽  
D Pauli ◽  
A P Mahowald
Keyword(s):  
Drosophila Melanogaster ◽  
Sex Determination ◽  
Sexual Identity ◽  
Gene Product ◽  
Germ Cells ◽  
Germ Line ◽  
Partial Transformation ◽  
Loss Of Function ◽  
Lethal Allele ◽  
Sex Lethal

Abstract Zygotically contributed ovo gene product is required for the survival of female germ cells in Drosophila melanogaster. Trans-allelic combinations of weak and dominant ovo mutations (ovoD) result in viable germ cells that appear to be partially transformed from female to male sexual identity. The ovoD2 mutation is partially suppressed by many Sex-lethal alleles that affect the soma, while those that affect only the germ line fail to interact with ovoD2. One of two loss-of-function ovo alleles is suppressed by a loss-of-function Sex-lethal allele. Because ovo mutations are germ line dependent, it is likely that ovo is suppressed by way of communication between the somatic and germ lines. A loss-of-function allele of ovo is epistatic to germ line dependent mutations in Sex-lethal. The germ line dependent sex determination mutation, sans fille, and ovoD mutations show a dominant synergistic interaction resulting in partial transformation of germ line sexual identity. The ovo locus appears to be involved in germ line sex determination and is linked in some manner to sex determination in the soma.

scholarly journals Characterization of Alternative Splicing (AS) Events during Chicken (Gallus gallus) Male Germ-Line Stem Cell Differentiation with Single-Cell RNA-seq

Animals ◽  
2021 ◽  
Vol 11 (5) ◽  
pp. 1469
Author(s):  
Changhua Sun ◽  
Kai Jin ◽  
Qisheng Zuo ◽  
Hongyan Sun ◽  
Jiuzhou Song ◽  
...  
Keyword(s):  
Stem Cells ◽  
Stem Cell ◽  
Alternative Splicing ◽  
Cell Differentiation ◽  
Germ Cell ◽  
Germ Cells ◽  
Germ Line ◽  
Rna Seq ◽  
Germ Cell Differentiation ◽  
Genome Wide

Alternative splicing (AS) is a ubiquitous, co-transcriptional, and post-transcriptional regulation mechanism during certain developmental processes, such as germ cell differentiation. A thorough understanding of germ cell differentiation will help us to open new avenues for avian reproduction, stem cell biology, and advances in medicines for human consumption. Here, based on single-cell RNA-seq, we characterized genome-wide AS events in manifold chicken male germ cells: embryonic stem cells (ESCs), gonad primordial germ cells (gPGCs), and spermatogonia stem cells (SSCs). A total of 38,494 AS events from 15,338 genes were detected in ESCs, with a total of 48,955 events from 14,783 genes and 49,900 events from 15,089 genes observed in gPGCs and SSCs, respectively. Moreover, this distribution of AS events suggests the diverse splicing feature of ESCs, gPGCs, and SSCs. Finally, several crucial stage-specific genes, such as NANOG, POU5F3, LIN28B, BMP4, STRA8, and LHX9, were identified in AS events that were transmitted in ESCs, gPGCs, and SSCs. The gene expression results of the RNA-seq data were validated by qRT-PCR. In summary, we provided a comprehensive atlas of the genome-wide scale of the AS event landscape in male chicken germ-line cells and presented its distribution for the first time. This research may someday improve treatment options for men suffering from male infertility.

Sex determination in the germ line of Drosophila depends on genetic signals and inductive somatic factors

Development ◽  
1989 ◽  
Vol 107 (3) ◽  
pp. 505-518 ◽  
Author(s):  
R. Nothiger ◽  
M. Jonglez ◽  
M. Leuthold ◽  
P. Meier-Gerschwiler ◽  
T. Weber
Keyword(s):  
Sex Determination ◽  
Germ Cells ◽  
Germ Line ◽  
The State ◽  
Loss Of Function ◽  
X Chromosomes ◽  
Constitutive Mutation ◽  
Sex Lethal ◽  
Double Sex ◽  
State Of Activity

We have analyzed the mechanism of sex determination in the germ line of Drosophila by manipulating three parameters: (1) the ratio of X-chromosomes to sets of autosomes (X:A); (2) the state of activity of the gene Sex-lethal (Sxl), and (3) the sex of the gonadal soma. To this end, animals with a ratio of 2X:2A and 2X:3A were sexually transformed into pseudomales by mutations at the sex-determining genes Sxl (Sex-lethal), tra (transformer), tra-2 (transformer-2), or dsx (double-sex). Animals with the karyotype 2X;3A were also transformed into pseudofemales by the constitutive mutation SxlM1. The sexual phenotype of the gonads and of the germ cells was assessed by phase-contrast microscopy. Confirming the conclusions of Steinmann-Zwicky et al. (Cell 57, 157, 1989), we found that all three parameters affect sex determination in germ cells. In contrast to the soma in which sex determination is completely cell-autonomous, sex determination in the germ line has a non-autonomous component inasmuch as the sex of the soma can influence the sexual pathway of the germ cells. Somatic induction has a clear effect on 2X;2A germ cells that carry a Sxl+ allele. These cells, which form eggs in an ovary, can enter spermatogenesis in testes. Mutations that cause partial loss of function or gain of function of Sxl thwart somatic induction and, independently of the sex of the soma, dictate spermatogenesis or oogenesis, respectively. Somatic induction has a much weaker effect on 2X;3A germ cells. This ratio is essentially a male signal for germ cells which consistently enter spermatogenesis in testes, even when they carry SxlM1. In a female soma, however, SxlM1 enables the 2X;3A germ cells to form almost normal eggs. Our results show that sex determination in the germ line is more complex than in the soma. They provide further evidence that the state of Sxl, the key gene for sex determination and dosage compensation in the soma, also determines the sex of the germ cells, and that, in the germ line, the state of activity of Sxl is regulated not only by the X:A ratio, but also by somatic inductive stimuli.

scholarly journals The sex determination master switch, Sex-lethal, responds to Hedgehog signaling in theDrosophilagermline

Development ◽  
2001 ◽  
Vol 128 (14) ◽  
pp. 2649-2660 ◽  
Author(s):  
Cynthia Vied ◽  
Jamila I. Horabin
Keyword(s):  
Sex Determination ◽  
Signaling Pathway ◽  
Germ Cells ◽  
Meiotic Recombination ◽  
Hedgehog Signaling ◽  
Nuclear Translocation ◽  
Hedgehog Signaling Pathway ◽  
Cubitus Interruptus ◽  
Protein Levels ◽  
Sex Lethal

Sex-lethal is the Drosophila melanogaster sex determination master switch. It is also required in female germ cells to control mitosis and meiotic recombination. As early germ cells mature, distinct changes in both Sex-lethal protein levels and localization occur. By manipulating the levels of Hedgehog and making germline clones of components in the hedgehog signaling pathway, we demonstrate that Hedgehog affects the nuclear translocation of Sex-lethal and the levels of the protein in early germ cells. This effect is mediated primarily through degradation. Consistent with the Hedgehog pathway regulating Sex-lethal, we find Sex-lethal in a complex with Fused and Costal-2, both downstream components of the pathway. This is the first demonstration that downstream components of the Hedgehog signaling pathway regulate a target other than Cubitus interruptus.

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