Disease relevance of xol-1

• Loss-of-function mutations in the X-linked gene xol-1 cause the feminization and death of XO animals (normally males) by shifting the sex determination and dosage compensation pathways toward their hermaphrodite modes [1].

High impact information on xol-1

• Moreover, sdc-2, a gene that must be repressed by xol-1 to ensure male development, may be a direct target of negative regulation by xol-1 [2].
• These results demonstrate that xol-1 functions as an early developmental switch to set the choice of sexual fate and suggest that assessment of the X/A ratio occurs only early in embryogenesis to determine sex [2].
• In xol-1 mutant XO embryos that activate the XX mode of dosage compensation and die from inappropriately low X chromosome transcript levels, DPY-27 becomes localized to X [3].
• The other uses the putative RNA-binding protein encoded by fox-1 to reduce the level of xol-1 protein [4].
• We demonstrate that the dose-sensitive signal elements on chromosome X control xol-1 through two different molecular mechanisms [4].

Biological context of xol-1

• XO-specific lethality most likely results from the reduction in X chromosome expression caused by xol-1 mutations [1].
• Specific genes termed X-signal elements, which are present on the X chromosome, act in a concerted dose-dependent fashion to regulate levels of the developmental switch gene xol-1 [5].
• Twenty-three mutations were isolated after chemical mutagenesis and found to fall into both expected classes (four dominant tra-1 mutations and eight recessive xol-1 mutations) and novel classes [6].

Regulatory relationships of xol-1

• Here we show the signal includes discrete, trans-acting autosomal signal elements (ASEs) that counter XSEs to coordinately control both sex determination and dosage compensation. sea-1, the first autosomal signal element, encodes a T-box transcription factor that opposes XSEs by activating transcription of xol-1 [7].

Other interactions of xol-1

• Additionally, fox-1(Delta) impairs male mating efficiency, which, we propose, represents another function of fox-1, independent of xol-1 and its role in sex determination [8].
• In XX hermaphrodites, accumulation of both her-1 transcripts is repressed by the sdc genes, which in turn are negatively regulated by the xol-1 gene [9].

References