Chapter 3 The Creation of Sexual Dimorphism in the Drosophila Soma

Camara, Nicole; Whitworth, Cale; Doren, Mark Van

doi:10.1016/s0070-2153(08)00403-1

Cited by 76 publications

(96 citation statements)

References 208 publications

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“…DSX M and DSX F share identical DNA-binding domains, but have different C termini (Burtis et al, 1991;Erdman and Burtis, 1993). The DSX proteins specify nearly all somatic sexual differences outside the nervous system, as well as several nervous system sexual dimorphisms (Lee et al, 2002;Sander and Arbeitman, 2008;Robinett et al, 2010;Rideout et al, 2010;Mellert et al, 2010) (for reviews, see Christiansen et al, 2002;Camara et al, 2008).…”

Section: Introductionmentioning

confidence: 99%

“…Although some genes whose activity levels are dependent on dsx have been identified by a candidate gene approach, most have been identified via plus/minus, microarray, SAGE or enhancer trapbased screens for genes expressed sex-differentially in the soma (Shirangi et al, 2009;Lebo et al, 2009;Chatterjee et al, 2011) (for reviews, see Christiansen et al, 2002;Camara et al, 2008). These screens identified dozens of genes whose activity levels are governed by dsx, but did not distinguish direct from indirect targets.…”

Section: Introductionmentioning

confidence: 99%

“…Studies of these dsx-regulated genes showed that the DSX proteins largely act by modulating in some tissues the activities of genes that are also used sex-nonspecifically in other tissues. The array of processes regulated by dsx is complex, as different genes are regulated by dsx in all cell and tissue types examined (for reviews, see Christiansen et al, 2002;Camara et al, 2008). Of the dsx-regulated genes that have been sufficiently characterized to distinguish likely direct and indirect targets, the vast majority are indirect targets (Arbeitman et al, 2004;Chapman and Wolfner, 1988;Wolfner, 1988).…”

Section: Introductionmentioning

confidence: 99%

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Direct targets of theD. melanogasterDSXF protein and the evolution of sexual development

2011

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SUMMARYUncovering the direct regulatory targets of doublesex (dsx) and fruitless (fru) is crucial for an understanding of how they regulate sexual development, morphogenesis, differentiation and adult functions (including behavior) in Drosophila melanogaster. Using a modified DamID approach, we identified 650 DSX-binding regions in the genome from which we then extracted an optimal palindromic 13 bp DSX-binding sequence. This sequence is functional in vivo, and the base identity at each position is important for DSX binding in vitro. In addition, this sequence is enriched in the genomes of D. melanogaster (58 copies versus approximately the three expected from random) and in the 11 other sequenced Drosophila species, as well as in some other Dipterans. Twenty-three genes are associated with both an in vivo peak in DSX binding and an optimal DSX-binding sequence, and thus are almost certainly direct DSX targets. The association of these 23 genes with optimum DSX binding sites was used to examine the evolutionary changes occurring in DSX and its targets in insects.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Direct targets of theD. melanogasterDSXF protein and the evolution of sexual development

2011

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“…dsx and fru in turn encode sex-specific transcription factors that control male versus female morphology, physiology, and behavior (3,4). In addition, Sxl represses the male-specific dosage compensation system by regulating male-specific lethal 2 (msl-2) both at the level of alternative splicing and translational control (5).…”

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spenito is required for sex determination in Drosophila melanogaster

Dong

Perrimon

2015

Proc. Natl. Acad. Sci. U.S.A.

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Sex-lethal (Sxl) encodes the master regulator of the sex determination pathway in Drosophila and acts by controlling sex identity in both soma and germ line. In females Sxl maintains its own expression by controlling the alternative splicing of its own mRNA. Here, we identify a novel sex determination gene, spenito (nito) that encodes a SPEN family protein. Loss of nito activity results in stem cell tumors in the female germ line as well as female-to-male somatic transformations. We show that Nito is a ubiquitous nuclear protein that controls the alternative splicing of the Sxl mRNA by interacting with Sxl protein and pre-mRNA, suggesting that it is directly involved in Sxl auto-regulation. Given that SPEN family proteins are frequently mutated in cancers, our results suggest that these factors might be implicated in tumorigenesis through splicing regulation.germ-line stem cell | sex determination | alternative splicing S ex determination in Drosophila is under the control of the master regulatory gene Sex-lethal (Sxl) (1). Sxl acts downstream of the X-chromosome counting mechanism and encodes a female-specific RNA binding protein. Once activated, Sxl maintains its own expression by regulating the alternative splicing of its pre-mRNA. Sxl controls female fate by controlling somatic and germ-line sex identity as well as dosage compensation (2). In female somatic cells, Sxl controls the alternative splicing of transformer (tra), which together with transformer2 (tra2) controls the alternative splicing of doublesex (dsx) and fruitless (fru). dsx and fru in turn encode sex-specific transcription factors that control male versus female morphology, physiology, and behavior (3, 4). In addition, Sxl represses the male-specific dosage compensation system by regulating male-specific lethal 2 (msl-2) both at the level of alternative splicing and translational control (5

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“…In Drosophila melanogaster, the molecular mechanisms leading to the sex-specific and temporally and spatially restricted deployment of the transcription factors encoded by the terminal genes in the sex-determination regulatory hierarchy, doublesex (dsx) and fruitless (fru), have been well documented (1)(2)(3)(4). In addition, although it has been established that the FRU M and DSX M and DSX F proteins control nearly all aspects of somatic sexual differentiation, including anatomical and behavioral differences, much less is known about the direct target genes through which these transcription factors act (2,3,(5)(6)(7)(8)(9)(10)(11).…”

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confidence: 99%

Constraints on the evolution of a doublesex target gene arising from doublesex’s pleiotropic deployment

Luo

Baker

2015

Proc. Natl. Acad. Sci. U.S.A.

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"Regulatory evolution," that is, changes in a gene's expression pattern through changes at its regulatory sequence, rather than changes at the coding sequence of the gene or changes of the upstream transcription factors, has been increasingly recognized as a pervasive evolution mechanism. Many somatic sexually dimorphic features of Drosophila melanogaster are the results of gene expression regulated by the doublesex (dsx) gene, which encodes sex-specific transcription factors (DSX F in females and DSX M in males). Rapid changes in such sexually dimorphic features are likely a result of changes at the regulatory sequence of the target genes. We focused on the Flavin-containing monooxygenase-2 (Fmo-2) gene, a likely direct dsx target, to elucidate how sexually dimorphic expression and its evolution are brought about. We found that dsx is deployed to regulate the Fmo-2 transcription both in the midgut and in fat body cells of the spermatheca (a female-specific tissue), through a canonical DSX-binding site in the Fmo-2 regulatory sequence. In the melanogaster group, Fmo-2 transcription in the midgut has evolved rapidly, in contrast to the conserved spermathecal transcription. We identified two cis-regulatory modules (CRM-p and CRM-d) that direct sexually monomorphic or dimorphic Fmo-2 transcription, respectively, in the midguts of these species. Changes of Fmo-2 transcription in the midgut from sexually dimorphic to sexually monomorphic in some species are caused by the loss of CRM-d function, but not the loss of the canonical DSX-binding site. Thus, conferring transcriptional regulation on a CRM level allows the regulation to evolve rapidly in one tissue while evading evolutionary constraints posed by other tissues.sex determination | transcription factors | DNA binding site | evolution H ow sex-specific characteristics are generated during development, what roles they have in the biology of an organism, and how they have evolved are fundamental questions in biology. In Drosophila melanogaster, the molecular mechanisms leading to the sex-specific and temporally and spatially restricted deployment of the transcription factors encoded by the terminal genes in the sex-determination regulatory hierarchy, doublesex (dsx) and fruitless (fru), have been well documented (1-4). In addition, although it has been established that the FRU M and DSX M and DSX F proteins control nearly all aspects of somatic sexual differentiation, including anatomical and behavioral differences, much less is known about the direct target genes through which these transcription factors act (2, 3, 5-11).It has been increasingly recognized that evolutionary significant changes in gene expression are often a result of mutations in the regulatory sequences of genes, rather than in their coding sequences (12). Furthermore, it has been noted that evolutionary changes are most likely in the cis-acting regulatory elements of the downstream targets of transcription factors, rather than in the genes encoding the transcription factors (13,14). This finding...

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Chapter 3 The Creation of Sexual Dimorphism in the Drosophila Soma

Cited by 76 publications

References 208 publications

Direct targets of theD. melanogasterDSXF protein and the evolution of sexual development

Direct targets of theD. melanogasterDSXF protein and the evolution of sexual development

spenito is required for sex determination in Drosophila melanogaster

Constraints on the evolution of a doublesex target gene arising from doublesex’s pleiotropic deployment

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