High impact information on dpy-5

• Genetic analysis of the nematode Caenorhabditis elegans reveals that all dpy-5 alleles are dominant suppressors of bli-4 blistering [1].
• RT-PCR analysis and a dpy-5::gfp fusion show that dpy-5 is expressed only in hypodermal cells at all post-embryonic life-cycle stages [1].
• Molecular cloning of dpy-5 establishes that it encodes a cuticle procollagen, defects in which are responsible for the short-body, dumpy phenotype [1].
• The same mutations also suppress certain alleles of another sex determination gene, tra-1, and of a morphogenetic gene, dpy-5 [2].
• The fraction of essential genes that present relatively large targets for EMS was highest within the central cluster (dpy-5 to unc-13) [3].

Biological context of dpy-5

• Essential genes were identified in the 1.5-map unit dpy-5 unc-13 region of chromosome I in the Caenorhabditis elegans genome by rescuing lethal mutations using the duplication sDp2 [4].
• A second duplication, sDp2, is a duplication of approximately 15 map units of the left portion of the linkage group. sDp2 was not observed to recombine with the normal homologue but did suppress exchange between the two normal homologues in a sDp2/ ++/ dpy-5 unc-35 heterozygote [5].
• Alignment of the genetic and physical maps in the dpy-5 bli-4 (I) region of C. elegans by the serial cosmid rescue of lethal mutations [6].

Associations of dpy-5 with chemical compounds

• Recombination frequency increased approximately twofold across the dpy-5-unc-13 interval after treatment with 2000 rads (1 rad = 10 mGy) of cobalt 60 gamma radiation [7].

Other interactions of dpy-5

• The gene maps on LGI, 0.4 map units from dpy-5 on the unc-11 side [8].

References