Worm Breeder's Gazette 13(4): 82 (October 1, 1994)
These abstracts should not be cited in bibliographies. Material contained herein should be treated as personal communication and should be cited as such only with the consent of the author.
Dept. of Biological Sciences, Columbia University, NY, NY 10027
The gene mec-6 is needed for the function of a set of touch receptor neurons (ALMs, PLMs, AVM and PVM). In addition, its was found that recessive mutations in mec-6 are able to suppress neuronal degenerations caused by dominant mutations in the genes deg-1 , mec-4 ,and mec-10 .These three genes all belong to a family of genes encoding degenerin protein. Based on the phenotype of the dominant mutations and the similarities of the degenerins to the components of the vertebrate amiloride-sensitive sodium channel, it is likely that the degenerins form membrane channels that can mutate to cause neuronal degenerations. One attractive model is that MEC-4 and MEC-10 help to form the mechanosensory channel in the touch receptor cells. In rat, the amiloride-sensitive sodium channel is made of three different degenerin-like subunits. We have investigated whether a third degenerin subunit is found in the touch cells. The best candidate for such a component is the mec-6 protein product. We have found an apparent degenerin homologue that maps to the mec-6 region on chromosome I. Using degenerative oligos that encode highly conserved regions of the degenerin gene family, we were able to PCR amplify a small fragment from the cosmid W01A8 that shares sequence homology with the degenerins. In addition, we cloned a 1.3kb genomic fragment that includes this region and found that this fragment detects a deletion in animals with the mec-6 ( u450 )gamma-ray mutation. Several transcripts were detected on a northern blot using this genomic fragment as probe. We are testing whether these transcripts are absent in the mec-6 ( u450 )animals. It seems likely that this degenerin is the mec-6 gene.