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      Are homologies in vertebrate sex determination due to shared ancestry or to limited options?

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      Author(s): 1 , , 2
      Publication date (Electronic):
      Journal: Genome Biology
      Publisher: BioMed Central

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          Abstract

          The bewildering array of different sex-determination systems in vertebrates is built on a common set of genes and chromosomes.

          Abstract

          The same candidate genes and the same autosomes are repeatedly used as sex chromosomes in vertebrates. Are these systems identical by descent, or are some genes or chromosomes intrinsically better at triggering the first steps of sex determination?

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          Most cited references67

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          DMY is a Y-specific DM-domain gene required for male development in the medaka fish.

          Masaru Matsuda, Yoshitaka Nagahama, Ai Shinomiya … (2002)
          Although the sex-determining gene Sry has been identified in mammals, no comparable genes have been found in non-mammalian vertebrates. Here, we used recombinant breakpoint analysis to restrict the sex-determining region in medaka fish (Oryzias latipes) to a 530-kilobase (kb) stretch of the Y chromosome. Deletion analysis of the Y chromosome of a congenic XY female further shortened the region to 250 kb. Shotgun sequencing of this region predicted 27 genes. Three of these genes were expressed during sexual differentiation. However, only the DM-related PG17 was Y specific; we thus named it DMY. Two naturally occurring mutations establish DMY's critical role in male development. The first heritable mutant--a single insertion in exon 3 and the subsequent truncation of DMY--resulted in all XY female offspring. Similarly, the second XY mutant female showed reduced DMY expression with a high proportion of XY female offspring. During normal development, DMY is expressed only in somatic cells of XY gonads. These findings strongly suggest that the sex-specific DMY is required for testicular development and is a prime candidate for the medaka sex-determining gene.
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            Sex determination involves synergistic action of SRY and SF1 on a specific Sox9 enhancer.

            Ryohei Sekido, Robin Lovell-Badge (2008)
            The mammalian Y chromosome acts as a dominant male determinant as a result of the action of a single gene, Sry, whose role in sex determination is to initiate testis rather than ovary development from early bipotential gonads. It does so by triggering the differentiation of Sertoli cells from supporting cell precursors, which would otherwise give follicle cells. The related autosomal gene Sox9 is also known from loss-of-function mutations in mice and humans to be essential for Sertoli cell differentiation; moreover, its abnormal expression in an XX gonad can lead to male development in the absence of Sry. These genetic data, together with the finding that Sox9 is upregulated in Sertoli cell precursors just after SRY expression begins, has led to the proposal that Sox9 could be directly regulated by SRY. However, the mechanism by which SRY action might affect Sox9 expression was not understood. Here we show that SRY binds to multiple elements within a Sox9 gonad-specific enhancer in mice, and that it does so along with steroidogenic factor 1 (SF1, encoded by the gene Nr5a1 (Sf1)), an orphan nuclear receptor. Mutation, co-transfection and sex-reversal studies all point to a feedforward, self-reinforcing pathway in which SF1 and SRY cooperatively upregulate Sox9 and then, together with SF1, SOX9 also binds to the enhancer to help maintain its own expression after that of SRY has ceased. Our results open up the field, permitting further characterization of the molecular mechanisms regulating sex determination and how they have evolved, as well as how they fail in cases of sex reversal.
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              The avian Z-linked gene DMRT1 is required for male sex determination in the chicken.

              Craig A. Smith, Kelly Roeszler, Thomas Ohnesorg … (2009)
              Sex in birds is chromosomally based, as in mammals, but the sex chromosomes are different and the mechanism of avian sex determination has been a long-standing mystery. In the chicken and all other birds, the homogametic sex is male (ZZ) and the heterogametic sex is female (ZW). Two hypotheses have been proposed for the mechanism of avian sex determination. The W (female) chromosome may carry a dominant-acting ovary determinant. Alternatively, the dosage of a Z-linked gene may mediate sex determination, two doses being required for male development (ZZ). A strong candidate avian sex-determinant under the dosage hypothesis is the conserved Z-linked gene, DMRT1 (doublesex and mab-3-related transcription factor 1). Here we used RNA interference (RNAi) to knock down DMRT1 in early chicken embryos. Reduction of DMRT1 protein expression in ovo leads to feminization of the embryonic gonads in genetically male (ZZ) embryos. Affected males show partial sex reversal, characterized by feminization of the gonads. The feminized left gonad shows female-like histology, disorganized testis cords and a decline in the testicular marker, SOX9. The ovarian marker, aromatase, is ectopically activated. The feminized right gonad shows a more variable loss of DMRT1 and ectopic aromatase activation, suggesting differential sensitivity to DMRT1 between left and right gonads. Germ cells also show a female pattern of distribution in the feminized male gonads. These results indicate that DMRT1 is required for testis determination in the chicken. Our data support the Z dosage hypothesis for avian sex determination.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Genome Biol
                Title: Genome Biology
                Publisher: BioMed Central
                ISSN (Print): 1465-6906
                ISSN (Electronic): 1465-6914
                Publication date (Print): 2010
                Publication date (Electronic): 30 April 2010
                Publication date PMC-release: 30 April 2011
                Volume: 11
                Issue: 4
                Page: 205
                Affiliations
                [1 ]Research School of Biology, the Australian National University, Canberra, ACT 0200, Australia
                [2 ]Division of Human Biology, Fred Hutchinson Cancer Research Center, Seattle, WA 98109, USA
                Article
                Publisher ID: gb-2010-11-4-205
                DOI: 10.1186/gb-2010-11-4-205
                PMC ID: 2884537
                PubMed ID: 20441602
                SO-VID: 9dba0d21-eb7f-45a9-ac02-f742ba75a23c
                Copyright © Copyright ©2010 BioMed Central Ltd
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                Subject: Review

                ScienceOpen disciplines: Genetics
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                ScienceOpen disciplines: Genetics

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