Alteration in cellular acetylcholine influences dauer formation in Caenorhabditis elegans.
Altered acetylcholine (Ach) homeostasis is associated with loss of viability in flies, developmental defects in mice, and cognitive deficits in human. Here, we assessed the importance of Ach in Caenorhabditis elegans development, focusing on the role of Ach during dauer formation. We found that dauer formation was disturbed in choline acetyltransferase (cha-1) and acetylcholinesterase (ace) mutants defective in Ach biosynthesis and degradation, respectively. When examined the potential role of G-proteins in dauer formation, goa-1 and egl-30 mutant worms, expressing mutated versions of mammalian G(o) and G(q) homolog, respectively, showed some abnormalities in dauer formation. Using quantitative mass spectrometry, we also found that dauer larvae had lower Ach content than did reproductively grown larvae. In addition, a proteomic analysis of acetylcholinesterase mutant worms, which have excessive levels of Ach, showed differential expression of metabolic genes. Collectively, these results indicate that alterations in Ach release may influence dauer formation in C. elegans.
Yonsei Proteome Research Center, College of Life Science and Biotechnology, World Class University Program, Graduate School, Yonsei University, Seoul 120-749, Korea.
Jeeyong
J
Lee
Yonsei Proteome Research Center, College of Life Science and Biotechnology, World Class University Program, Graduate School, Yonsei University, Seoul 120-749, Korea.
Kwang-Youl
KY
Kim
Yonsei Proteome Research Center, College of Life Science and Biotechnology, World Class University Program, Graduate School, Yonsei University, Seoul 120-749, Korea; Department of Biochemistry and Department of Integrated Omics for Biomedical Science, College of Life Science and Biotechnology, World Class University Program, Graduate School, Yonsei University, Seoul 120-749, Korea.
Young-Ki
YK
Paik
D000109:Acetylcholine / Q000032:analysis / Q000378:metabolism*; D000110:Acetylcholinesterase / Q000235:genetics / Q000378:metabolism; D000818:Animals; D017173:Caenorhabditis elegans / Q000254:growth & development / Q000378:metabolism*; D029742:Caenorhabditis elegans Proteins / Q000235:genetics / Q000378:metabolism; D002795:Choline O-Acetyltransferase / Q000235:genetics / Q000378:metabolism; D015180:Electrophoresis, Gel, Two-Dimensional; D019206:GTP-Binding Protein alpha Subunits, Gi-Go / Q000235:genetics / Q000378:metabolism; D043802:GTP-Binding Protein alpha Subunits, Gq-G11 / Q000235:genetics / Q000378:metabolism; D007814:Larva / Q000378:metabolism; D013058:Mass Spectrometry; D009154:Mutation
D029742:Caenorhabditis elegans Proteins; C479565:Egl-30 protein, C elegans; C516620:GOA-1 protein, C elegans; D002795:Choline O-Acetyltransferase; D000110:Acetylcholinesterase; D019206:GTP-Binding Protein alpha Subunits, Gi-Go; D043802:GTP-Binding Protein alpha Subunits, Gq-G11; D000109:Acetylcholine