Functions of the Caenorhabditis elegans Regulatory Myosin Light Chain Genes mlc-1 and mlc-2

摘要

Caenorhabditis elegans contains two muscle regulatory myosin light chain genes, mlc-1 and mlc-2. To determine their in vivo roles, we identified deletions that eliminate each gene individually and both genes in combination. Functions of mlc-1 are redundant to those of mlc-2 in both body-wall and pharyngeal muscle. mlc-1 ( 0 ) mutants are wild type, but mlc-1 ( 0 ) mlc-2 ( 0 ) double mutants arrest as incompletely elongated L1 larvae, having both pharyngeal and body-wall muscle defects. Transgenic copies of either mlc-1 (+) or mlc-2 (+) rescue all defects of mlc-1 ( 0 ) mlc-2 ( 0 ) double mutants. mlc-2 is redundant to mlc-1 in body-wall muscle, but mlc-2 performs a nearly essential role in the pharynx. Approximately 90% of mlc-2 ( 0 ) hermaphrodites arrest as L1 larvae due to pharyngeal muscle defects. Lethality of mlc-2 ( 0 ) mutants is sex specific, with mlc-2 ( 0 ) males being essentially wild type. Four observations suggest that hermaphrodite-specific lethality of mlc-2 ( 0 ) mutants results from insufficient expression of the X -linked mlc-1 (+) gene in the pharynx. First, mlc-1 ( 0 ) mlc-2 ( 0 ) double mutants are fully penetrant L1 lethals in both hermaphrodites and males. Second, in situ localization of mlc mRNAs demonstrates that both mlc-1 and mlc-2 are expressed in the pharynx. Third, transgenic copies of either mlc-1 (+) or mlc-2 (+) rescue the pharyngeal defects of mlc-1 ( 0 ) mlc-2 ( 0 ) hermaphrodites. Fourth, a mutation of the dosage compensation gene sdc-3 suppresses hermaphrodite-specific lethality of mlc-2 ( 0 ) mutants.