Sex-specific transcriptional regulation of the C. elegans sex-determining gene her-1

Trent, Carol; Purnell, Beverly A.; Gavinski, Sheri; Hageman, J. M.; Chamblin, Caroline; Wood, William B.

doi:10.1016/0925-4773(91)90090-s

Cited by 74 publications

(59 citation statements)

References 29 publications

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“…her-1 is one of the few genes in the sex-determination pathway that is controlled at the level of transcription and acts downstream of xol-1, making it an appropriate gene to monitor sex-1 function (Trent et al 1991). her-1 is repressed directly through binding of SDC proteins to the promoter and second intron (Chu et al 2002).…”

Section: Resultsmentioning

confidence: 99%

“…her-1 is repressed directly through binding of SDC proteins to the promoter and second intron (Chu et al 2002). The difference in her-1 transcript levels between XO and XX animals is estimated to be $20-fold (Trent et al 1991). Using qRT-PCR, we found that normalized her-1 transcript levels were elevated 6.5-fold in sex-1 mutants (P , 0.01) and 4.6-fold in xol-1 sex-1 mutants (P , 0.01), consistent with the XSE-independent function of sex-1 acting downstream of xol-1 and upstream of her-1 (Table 7).…”

Section: Resultsmentioning

confidence: 99%

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Revisiting the X:A Signal That Specifies Caenorhabditis elegans Sexual Fate

2007

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In Caenorhabditis elegans, sex is determined by the opposing actions of X-signal elements (XSEs) and autosomal signal elements (ASEs), which communicate the ratio of X chromosomes to sets of autosomes (X:A signal). This study delves more deeply into the mechanism by which XSEs transmit X chromosome dose. We determined the relative contributions of individual XSEs to the X:A signal and showed the order of XSE strength to be sex-1 . sex-2 . fox-1 . ceh-39 $ region 1 XSE. sex-1 exerts a more potent influence on sex determination and dosage compensation than any other XSE by functioning in two separate capacities in the pathway: sex-1 acts upstream as an XSE to repress xol-1 and downstream as an activator of hermaphrodite development and dosage compensation. Furthermore, the process of dosage compensation affects expression of the very XSEs that control it; XSEs become fully dosage compensated once sex is determined. The X:A signal is then equivalent between XO and XX animals, causing sexual differentiation to be controlled by genes downstream of xol-1 in the sex-determination pathway. Prior to the onset of dosage compensation, the difference in XSE expression between XX and XO embryos appears to be greater than twofold, making X chromosome counting a robust process.

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Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

Revisiting the X:A Signal That Specifies Caenorhabditis elegans Sexual Fate

2007

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“…In addition to activating dosage compensation, SDC proteins induce hermaphrodite sexual differentiation by repressing transcription of the male-specific, autosomal gene her-1 (Chu et al, 2002;Dawes et al, 1999;DeLong et al, 1993;Trent et al, 1991). SDC proteins repress her-1 transcription 20-fold by binding to three separate regulatory regions within the gene (Chu et al, 2002).…”

Section: Dpy-21 Participates Directly In Chromosome-wide Repression Bmentioning

confidence: 99%

Recruitment ofC. elegansdosage compensation proteins for gene-specific versus chromosome-wide repression

Yonker

Meyer

2003

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In C. elegans, an X-chromosome-wide regulatory process compensates for the difference in X-linked gene dose between males (XO) and hermaphrodites(XX) by equalizing levels of X-chromosome transcripts between the sexes. To achieve dosage compensation, a large protein complex is targeted to the X chromosomes of hermaphrodites to reduce their expression by half. This repression complex is also targeted to a single autosomal gene, her-1. By silencing this male-specific gene, the complex induces hermaphrodite sexual development. Our analysis of the atypical dosage compensation gene dpy-21 revealed the first molecular differences in the complex that achieves gene-specific versus chromosome-wide repression. dpy-21 mutations, shown here to be null, cause elevated X-linked gene expression in XX animals, but unlike mutations in other dosage compensation genes, they do not cause extensive XX-specific lethality or disrupt the stability or targeting of the dosage compensation complex to X. Nonetheless,DPY-21 is a member of the dosage compensation complex and localizes to X chromosomes in a hermaphrodite-specific manner. However, DPY-21 is the first member of the dosage compensation complex that does not also associate with her-1. In addition to a difference in the composition of the complex at her-1 versus X, we also found differences in the targeting of the complex to these sites. Within the complex, SDC-2 plays the lead role in recognizing X-chromosome targets, while SDC-3 plays the lead in recognizing her-1 targets.

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“…In the sex-determination pathway, the SDC proteins downregulate the autosomal gene her-1 (hermaphroditization of XO animals) (Trent et al, 1991;Dawes et al, 1999;Chu et al, 2002). her-1 encodes a secreted protein that binds to and inhibits the transmembrane receptor product of tra-2 (sexual transformer) (Hodgkin, 1980).…”

Section: Introductionmentioning

confidence: 99%

xol-1, the master sex-switch gene in C. elegans, is a transcriptional target of the terminal sex-determining factor TRA-1

et al. 2009

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In the nematode Caenorhabditis elegans, sex is determined by the ratio of X chromosomes to sets of autosomes: XX animals (2X:2A1.0) develop as hermaphrodites and XO animals (1X:2A0.5) develop as males. TRA-1, the worm ortholog of Drosophila Cubitus interruptus and mammalian Gli (Glioma-associated homolog) proteins, is the terminal transcription factor of the C. elegans sex-determination pathway, which specifies hermaphrodite fate by repressing male-specific genes. Here we identify a consensus TRA-1 binding site in the regulatory region of xol-1, the master switch gene controlling sex determination and dosage compensation. xol-1 is normally expressed in males, where it promotes male development and prevents dosage compensation. We show that TRA-1 binds to the consensus site in the xol-1 promoter in vitro and inhibits the expression of xol-1 in XX animals in vivo. Furthermore, inactivation of tra-1 enhances, whereas hyperactivation of tra-1 suppresses, lethality in animals with elevated xol-1 activity. These data imply the existence of a regulatory feedback loop within the C. elegans sex-determination and dosagecompensation cascade that ensures the accurate dose of X-linked genes in cells destined to adopt hermaphrodite fate.

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Sex-specific transcriptional regulation of the C. elegans sex-determining gene her-1

Cited by 74 publications

References 29 publications

Revisiting the X:A Signal That Specifies Caenorhabditis elegans Sexual Fate

Revisiting the X:A Signal That Specifies Caenorhabditis elegans Sexual Fate

Recruitment ofC. elegansdosage compensation proteins for gene-specific versus chromosome-wide repression

xol-1, the master sex-switch gene in C. elegans, is a transcriptional target of the terminal sex-determining factor TRA-1

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