High impact information on dpy-21

• Reduction in the activity of either dpy-21, dpy-27, or dpy-28 results in the overexpression of X-specific genes, 2- to 3-fold above wild-type levels [1].
• We show that there is dosage compensation of transcript levels for these two genes between XX hermaphrodites and X0 males and that a mutation in the dpy-21 gene, postulated from genetic analysis to be involved in control of X chromosome expression, can affect these transcript levels in the manner predicted [2].
• However, we observe the dpy-21 effects only at some stages of the life cycle and not at others [2].
• In addition we show that recessive mutations in two autosomal genes, dpy-21 V and dpy-26 IV, suppress the phenotypes resulting from the X-linked hypomorphic mutations, but not the phenotypes resulting from comparable autosomal hypomorphic mutations [3].
• Additionally, in the case of dpy-21 we correlate the change in phenotypic expression of lin-14 with a corresponding change in the lin-14 mRNA transcript level [4].

Biological context of dpy-21

• Recessive mutant alleles at the autosomal dpy-21 locus of C. elegans cause a dumpy phenotype in XX animals but not in XO animals [5].
• This result strongly suggests that the dpy-21 and dpy-26 mutations cause increased X expression, implying that the normal function of these genes may be to lower the expression of X-linked genes [3].
• Our results show that the 5S rRNA gene cluster maps between unc-76 and dpy-21 on the right arm of linkage group V. This genetic localization provides a linkage group V "landmark" with which to localize other cloned sequences by in situ hybridization [6].

Regulatory relationships of dpy-21

• All dpy-21 alleles show hermaphroditization effects in XO males that carry a duplication of part of the X chromosome and also partially suppress a transformer (tra-1) mutation that converts XX animals into males [5].

References