Sex-lethal, A Link between Sex Determination and Sexual Differentiation in Drosophila melanogaster

1985 ◽  
Vol 50 (0) ◽  
pp. 595-604 ◽  
Author(s):  
E.M. Maine ◽  
H.K. Salz ◽  
P. Schedl ◽  
T.W. Cline
Keyword(s):  
Drosophila Melanogaster ◽  
Sex Determination ◽  
Sexual Differentiation ◽  
Sex Lethal

A Theoretical Model for the Regulation of Sex-lethal, a Gene That Controls Sex Determination and Dosage Compensation in Drosophila melanogaster

Genetics ◽  
2003 ◽  
Vol 165 (3) ◽  
pp. 1355-1384
Author(s):  
Matthieu Louis ◽  
Liisa Holm ◽  
Lucas Sánchez ◽  
Marcelle Kaufman
Keyword(s):  
Drosophila Melanogaster ◽  
Theoretical Model ◽  
Sex Determination ◽  
Numerical Simulations ◽  
Cell Fate ◽  
Regulatory Gene ◽  
Experimental Studies ◽  
Formal Basis ◽  
Sex Lethal ◽  
Specific Regulation

Abstract Cell fate commitment relies upon making a choice between different developmental pathways and subsequently remembering that choice. Experimental studies have thoroughly investigated this central theme in biology for sex determination. In the somatic cells of Drosophila melanogaster, Sex-lethal (Sxl) is the master regulatory gene that specifies sexual identity. We have developed a theoretical model for the initial sex-specific regulation of Sxl expression. The model is based on the well-documented molecular details of the system and uses a stochastic formulation of transcription. Numerical simulations allow quantitative assessment of the role of different regulatory mechanisms in achieving a robust switch. We establish on a formal basis that the autoregulatory loop involved in the alternative splicing of Sxl primary transcripts generates an all-or-none bistable behavior and constitutes an efficient stabilization and memorization device. The model indicates that production of a small amount of early Sxl proteins leaves the autoregulatory loop in its off state. Numerical simulations of mutant genotypes enable us to reproduce and explain the phenotypic effects of perturbations induced in the dosage of genes whose products participate in the early Sxl promoter activation.

scholarly journals Regulation of behavioral and pheromonal aspects of sex determination in Drosophila melanogaster by the Sex-lethal gene.

Genetics ◽  
1989 ◽  
Vol 123 (3) ◽  
pp. 535-541 ◽  
Author(s):  
L Tompkins ◽  
S P McRobert
Keyword(s):  
Drosophila Melanogaster ◽  
Sexual Behavior ◽  
Sex Determination ◽  
Ectopic Expression ◽  
Lethal Gene ◽  
Gene Products ◽  
Morphological Aspects ◽  
Sex Lethal ◽  
Normal Males ◽  
Female Specific

Abstract We have shown that the Sex-lethal (Sxl) gene, which controls morphological aspects of sex determination in Drosophila melanogaster, also regulates sexual behavior. Chromosomal males that are hemizygous for a deletion of the entire Sxl locus perform normal courtship and synthesize the two courtship-inhibiting pheromones that normal males make. However, ectopic expression of female-specific Sex-lethal gene products drastically alters chromosomal males' ability to perform and elicit courtship and increases the probability that they will synthesize a courtship-stimulating pheromone or fail to synthesize one of the inhibitory pheromones. These observations suggest that male sexual behavior is a consequence of the Sxl gene's being functionally inactive in haplo-X flies.

scholarly journals Regulated splicing of the Drosophila sex-lethal male exon involves a blockage mechanism.

1993 ◽  
Vol 13 (3) ◽  
pp. 1408-1414 ◽  
Author(s):  
J I Horabin ◽  
P Schedl
Keyword(s):  
Drosophila Melanogaster ◽  
Alternative Splicing ◽  
Sex Determination ◽  
Splice Site ◽  
Feedback Loop ◽  
Splice Sites ◽  
Alternate Splicing ◽  
Sequence Context ◽  
Sex Lethal ◽  
Hodgkin Cell

In Drosophila melanogaster, sex determination in somatic cells is controlled by a cascade of genes whose expression is regulated by alternative splicing [B. S. Baker, Nature (London) 340:521-524, 1989; J. Hodgkin, Cell 56:905-906, 1989]. The master switch gene in this hierarchy is Sex-lethal. Sex-lethal is turned on only in females, and an autoregulatory feedback loop which controls alternative splicing maintains this state (L. R. Bell, J. I. Horabin, P. Schedl, and T. W. Cline, Cell 65:229-239, 1991; L. N. Keyes, T. W. Cline, and P. Schedl, Cell 68:933-943, 1992). Sex-lethal also promotes female differentiation by controlling the splicing of RNA from the next gene in the hierarchy, transformer. Sosnowski et al. (B. A. Sosnowski, J. M. Belote, and M. McKeown, Cell 58:449-459, 1989) have shown that the mechanism for generating female transformer transcripts is not through the activation of the alternative splice site but by the blockage of the default splice site. We have tested whether an activation or a blockage mechanism is involved in Sex-lethal autoregulation. The male exon of Sex-lethal with flanking splice sites was placed into the introns of heterologous genes. Our results support the blockage mechanism. The poly(U) run at the male exon 3' splice site is required for sex-specific splicing. However, unlike transformer, default splicing to the male exon is sensitive to the sequence context within which the exon resides. This and the observation that the splice signals at the exon are suboptimal are discussed with regard to alternate splicing.

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.

Molecular genetic aspects of sex determination in Drosophila melanogaster

Genome ◽  
1989 ◽  
Vol 31 (2) ◽  
pp. 638-645 ◽  
Author(s):  
B. S. Baker ◽  
K. Burtis ◽  
T. Goralski ◽  
W. Mattox ◽  
R. Nagoshi
Keyword(s):  
Drosophila Melanogaster ◽  
Sex Determination ◽  
Sexual Differentiation ◽  
Rna Processing ◽  
Molecular Basis ◽  
Rna Binding ◽  
Regulatory Genes ◽  
Regulatory State ◽  
Splice Acceptor ◽  
Regulatory Cascade

The molecular analyses of three of the regulatory genes (transformer (tra), doublesex (dsx), and transformer-2 (tra-2)) controlling sexual differentiation in Drosophila have demonstrated that the control of RNA processing has a major role in regulating somatic sexual differentiation. The activities of both the tra and dsx genes are controlled at the level of RNA processing. In the case of tra the use of different splice acceptor sites results in a functional transcript being produced only in females, whereas at dsx the use of different splice acceptor sites in the two sexes results in the production of transcripts that encode different proteins in males and females. The tra-2 gene has been shown to be necessary for the processing of the dsx pre-mRNA in females and the conceptual translation of a tra-2 cDNA shows that it encodes a protein with similarity to a family of RNA-binding proteins which includes known splicesome components. We previously suggested that the pattern of sexual differentiation and dosage compensation characteristic of a male was a default regulatory state. The findings reviewed here provide a molecular basis for this default expression in males as well as an insight into how females differ from males in control of the expression of these genes. For both the tra and dsx genes the molecular basis of their male (default) state of expression appears to be the processing of their transcripts by the housekeeping RNA splicing machinery. In females the specification of the alternative pattern of splicing at both tra and dsx is by the sex determination regulatory genes that function upstream of them in this regulatory cascade. It seems likely that the activities of these sex determination regulatory genes in females do not provide all of the information that is necessary for proper splicing of the transcripts of the genes downstream of them. Rather we imagine that the products of the Sxl, tra, and tra-2 genes are acting to impose a specificity on the basic cellular splicing machinery.Key words: Drosophila melanogaster, sex determination, sexual differentiation.

Sex-lethal, master and slave: a hierarchy of germ-line sex determination in Drosophila

Development ◽  
1993 ◽  
Vol 119 (3) ◽  
pp. 897-908 ◽  
Author(s):  
B. Oliver ◽  
Y.J. Kim ◽  
B.S. Baker
Keyword(s):  
Drosophila Melanogaster ◽  
Sex Determination ◽  
Ovarian Tumor ◽  
Germ Line ◽  
Female Sex ◽  
Somatic Signal ◽  
Female Germ Line ◽  
Sex Lethal ◽  
Female Specific ◽  
Genetic Hierarchy

Female sex determination in the germ line of Drosophila melanogaster is regulated by genes functioning in the soma as well as genes that function within the germ line. Genes known or suspected to be involved in germ-line sex determination in Drosophila melanogaster have been examined to determine if they are required upstream or downstream of Sex-lethal+, a known germ-line sex determination gene. Seven genes required for female-specific splicing of germ-line Sex-lethal+ pre-mRNA are identified. These results together with information about the tissues in which these genes function and whether they control sex determination and viability or just sex determination in the germ line have been used to deduce the genetic hierarchy regulating female germ-line sex determination. This hierarchy includes the somatic sex determination genes transformer+, transformer-2+ and doublesex+ (and by inference Sex-lethal+), which control a somatic signal required for female germ-line sex determination, and the germ-line ovarian tumor genes fused+, ovarian tumor+, ovo+, sans fille+, and Sex-lethal+, which are involved in either the reception or interpretation of this somatic sex determination signal. The fused+, ovarian tumor+, ovo+ and sans fille+ genes function upstream of Sex-lethal+ in the germ line.

Identification of regions interacting with ovoD mutations: potential new genes involved in germline sex determination or differentiation in Drosophila melanogaster.

Genetics ◽  
1995 ◽  
Vol 139 (2) ◽  
pp. 713-732 ◽  
Author(s):  
D Pauli ◽  
B Oliver ◽  
A P Mahowald
Keyword(s):  
Drosophila Melanogaster ◽  
Sex Determination ◽  
Sexual Identity ◽  
Ovarian Tumor ◽  
Biological Process ◽  
Genetic Interactions ◽  
New Genes ◽  
Sex Lethal ◽  
Germline Sex Determination

Abstract Only a few Drosophila melanogaster germline sex determination genes are known, and there have been no systematic screens to identify new genes involved in this important biological process. The ovarian phenotypes produced by females mutant for dominant alleles of the ovo gene are modified in flies with altered doses of other loci involved in germline sex determination in Drosophila (Sex-lethal+, sans fille+ and ovarian tumor+). This observation constitutes the basis for a screen to identify additional genes required for proper establishment of germline sexual identity. We tested 300 deletions, which together cover approximately 58% of the euchromatic portion of the genome, for genetic interactions with ovoD. Hemizygosity for more than a dozen small regions show interactions that either partially suppress or enhance the ovarian phenotypes of females mutant for one or more of the three dominant ovo mutations. These regions probably contain genes whose products act in developmental hierarchies that include ovo+ protein.

scholarly journals A genetic analysis of hermaphrodite, a pleiotropic sex determination gene in Drosophila melanogaster.

Genetics ◽  
1994 ◽  
Vol 136 (1) ◽  
pp. 195-207
Author(s):  
M A Pultz ◽  
G S Carson ◽  
B S Baker
Keyword(s):  
Drosophila Melanogaster ◽  
Genetic Analysis ◽  
Sex Determination ◽  
Temperature Sensitivity ◽  
Sexual Differentiation ◽  
Regulatory Genes ◽  
Temperature Sensitive ◽  
Partial Loss ◽  
Female Progeny ◽  
Regulatory Cascade

Abstract Sex determination in Drosophila is controlled by a cascade of regulatory genes. Here we describe hermaphrodite (her), a new component of this regulatory cascade with pleiotropic zygotic and maternal functions. Zygotically, her+ function is required for female sexual differentiation: when zygotic her+ function is lacking, females are transformed to intersexes. Zygotic her+ function may also play a role in male sexual differentiation. Maternally, her+ function is needed to ensure the viability of female progeny: a partial loss of her+ function preferentially kills daughters. In addition, her has both zygotic and maternal functions required for viability in both sexes. Temperature sensitivity prevails for all known her alleles and for all of the her phenotypes described above, suggesting that her may participate in an intrinsically temperature-sensitive process. This analysis of four her alleles also indicates that the zygotic and maternal components of of her function are differentially mutable. We have localized her cytologically to 36A3-36A11.

Regulated splicing of the Drosophila sex-lethal male exon involves a blockage mechanism

1993 ◽  
Vol 13 (3) ◽  
pp. 1408-1414
Author(s):  
J I Horabin ◽  
P Schedl
Keyword(s):  
Drosophila Melanogaster ◽  
Alternative Splicing ◽  
Sex Determination ◽  
Splice Site ◽  
Feedback Loop ◽  
Splice Sites ◽  
Alternate Splicing ◽  
Sequence Context ◽  
Sex Lethal ◽  
Hodgkin Cell

In Drosophila melanogaster, sex determination in somatic cells is controlled by a cascade of genes whose expression is regulated by alternative splicing [B. S. Baker, Nature (London) 340:521-524, 1989; J. Hodgkin, Cell 56:905-906, 1989]. The master switch gene in this hierarchy is Sex-lethal. Sex-lethal is turned on only in females, and an autoregulatory feedback loop which controls alternative splicing maintains this state (L. R. Bell, J. I. Horabin, P. Schedl, and T. W. Cline, Cell 65:229-239, 1991; L. N. Keyes, T. W. Cline, and P. Schedl, Cell 68:933-943, 1992). Sex-lethal also promotes female differentiation by controlling the splicing of RNA from the next gene in the hierarchy, transformer. Sosnowski et al. (B. A. Sosnowski, J. M. Belote, and M. McKeown, Cell 58:449-459, 1989) have shown that the mechanism for generating female transformer transcripts is not through the activation of the alternative splice site but by the blockage of the default splice site. We have tested whether an activation or a blockage mechanism is involved in Sex-lethal autoregulation. The male exon of Sex-lethal with flanking splice sites was placed into the introns of heterologous genes. Our results support the blockage mechanism. The poly(U) run at the male exon 3' splice site is required for sex-specific splicing. However, unlike transformer, default splicing to the male exon is sensitive to the sequence context within which the exon resides. This and the observation that the splice signals at the exon are suboptimal are discussed with regard to alternate splicing.

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