title: Mitochondrial ATP synthase controls larval development cell nonautonomously in Caenorhabditis elegans.
abstract: The mitochondrial respiratory chain is composed of five protein complexes capable of generating cellular energy in the form of ATP. Defects in mitochondrial energy production can result in a wide variety of diseases with tissue-specific effects. We previously have isolated a mutation in the atp-2 gene, which encodes the active site or beta-subunit of complex V in Caenorhabditis elegans. This atp-2(ua2) mutation is lethal, resulting in developmental arrest at the third larval stage (L3). In this report, we use mosaic analysis to identify the tissues in which atp-2 gene activity is dispensable for development past the L3 stage. The loss of atp-2 in any tissue can provoke arrest at the L3 stage. However, animals with a loss of the atp-2 gene in the ABa lineage, which gives rise to neuronal, pharyngeal, and hypodermal cells, and/or the E lineage, which gives rise to the intestinal cells, can occasionally develop past L3. Loss of atp-2 gene function in the lineages that give rise to the body muscles is invariably associated with developmental arrest. This finding suggests that the body muscles may play a key role in regulating development. We conclude that atp-2 functions cell nonautonomously in this developmental process. Our findings suggest that atp-2 is involved in the production or the regulation of a global, developmental signal required for the L3-to-L4 transition.
authors.affiliation: The Canadian Institutes of Health Membrane Protein Research Group, Department of Biochemistry, University of Alberta, Edmonton, Alberta, Canada.
authors.forename: William Y
authors.initials: WY
authors.lastname: Tsang
authors.forename: Bernard D
authors.initials: BD
authors.lastname: Lemire
mesh_terms: D000818:Animals; D017173:Caenorhabditis elegans / Q000196:embryology* / Q000201:enzymology*; D019070:Cell Lineage / Q000502:physiology; D018507:Gene Expression Regulation, Developmental; D015971:Gene Expression Regulation, Enzymologic; D005838:Genotype; D007814:Larva / Q000254:growth & development; D008928:Mitochondria / Q000201:enzymology; D025261:Mitochondrial Proton-Translocating ATPases / Q000235:genetics* / Q000378:metabolism*; D009030:Mosaicism; D009154:Mutation / Q000502:physiology; D010641:Phenotype
chemical_list: D025261:Mitochondrial Proton-Translocating ATPases