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Gene Review:

dpy-22 - Protein DPY-22

Caenorhabditis elegans

Meneely, P.M. et al., Yoda, A. et al., Wang, J.C. et al.

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High impact information on dpy-22

We found that the let-19 and dpy-22 mutants have defects in their T-cell lineage, and lineage analyses showed that the defects were caused by disruption in the asymmetry of the T-cell division [1].
In the let-19 and dpy-22 mutants, tlp-1, which is normally expressed asymmetrically between the T-cell daughters through the function of the Wnt pathway, was expressed symmetrically in both daughter cells [1].
Additionally, CeTRAP240/let-19(RNAi) in a CeTRAP230/dpy-22 mutant background produced a strong synthetic lethal phenotype [2].
Recessive mutations in two other dpy genes, dpy-22 X and dpy-23 X, increase the severity of phenotypes resulting from some X-linked hypomorphic mutations, although dpy-23 may affect the phenotypes resulting from the autosomal hypomorphs as well [3].

Biological context of dpy-22

Overall, our results establish specific roles of CeTRAP240/let-19 in C. elegans embryonic development and a functional interaction between CeTRAP240/let-19 and CeTRAP230/dpy-22 [2].

References

Components of the transcriptional Mediator complex are required for asymmetric cell division in C. elegans. Yoda, A., Kouike, H., Okano, H., Sawa, H. Development (2005) [Pubmed]
The Caenorhabditis elegans ortholog of TRAP240, CeTRAP240/let-19, selectively modulates gene expression and is essential for embryogenesis. Wang, J.C., Walker, A., Blackwell, T.K., Yamamoto, K.R. J. Biol. Chem. (2004) [Pubmed]
Genetic analysis of X-chromosome dosage compensation in Caenorhabditis elegans. Meneely, P.M., Wood, W.B. Genetics (1987) [Pubmed]

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