ABSTRACT
The fusion of the Caenorhabditis elegans uterine anchor cell (AC) with the uterine-seam cell (utse) is an excellent model system for studying cell-cell fusion, which is essential to animal development. We obtained an egg-laying defective (Egl) mutant in which the AC fails to fuse with the utse. This defect is highly specific: other aspects of utse development and other cell fusions appear to occur normally. We find that defect is due to a missense mutation in the nsf-1 gene, which encodes N-ethylmaleimide-sensitive factor (NSF), an intracellular membrane fusion factor. There are two NSF-1 isoforms, which are expressed in distinct tissues through two separate promoters. NSF-1L is expressed in the uterus, including the AC. We find that nsf-1 is required cell-autonomously in the AC for its fusion with the utse. Our results establish AC fusion as a paradigm for studying cell fusion at single cell resolution and demonstrate that the NSF ATPase is a key player in this process.
Subject(s)
Caenorhabditis elegans Proteins/metabolism , Ethylmaleimide/pharmacology , N-Ethylmaleimide-Sensitive Proteins/drug effects , N-Ethylmaleimide-Sensitive Proteins/metabolism , Uterus/cytology , Animals , Animals, Genetically Modified , Caenorhabditis elegans/drug effects , Caenorhabditis elegans/physiology , Caenorhabditis elegans Proteins/drug effects , Caenorhabditis elegans Proteins/genetics , Cell Fusion , Female , Membrane Glycoproteins/drug effects , Membrane Glycoproteins/genetics , Membrane Glycoproteins/metabolism , Mutation, Missense , N-Ethylmaleimide-Sensitive Proteins/genetics , Organ Specificity , Phenotype , Promoter Regions, Genetic , Uterus/drug effectsABSTRACT
We isolated egl-13 mutants in which the pi cells of the Caenorhabditis elegans uterus initially appeared to develop normally but then underwent an extra round of cell division. The data suggest that egl-13 is required for maintenance of the pi cell fate.
