Alteration in cellular acetylcholine influences dauer formation in Caenorhabditis elegans
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Altered acetylcholine (Ach) homeostasis is associated with lossof viability in flies, developmental defects in mice, andcognitive deficits in human. Here, we assessed the importanceof Ach in Caenorhabditis elegans development, focusing onthe role of Ach during dauer formation. We found that dauerformation was disturbed in choline acetyltransferase (cha-1)and acetylcholinesterase (ace) mutants defective in Achbiosynthesis and degradation, respectively. When examinedthe potential role of G-proteins in dauer formation, goa-1 andegl-30 mutant worms, expressing mutated versions ofmammalian Go and Gq homolog, respectively, showed someabnormalities in dauer formation. Using quantitative massspectrometry, we also found that dauer larvae had lower Achcontent than did reproductively grown larvae. In addition, aproteomic analysis of acetylcholinesterase mutant worms,which have excessive levels of Ach, showed differentialexpression of metabolic genes. Collectively, these resultsindicate that alterations in Ach release may influence dauerformation in C. elegans.
Abstract
Altered acetylcholine (Ach) homeostasis is associated with lossof viability in flies, developmental defects in mice, andcognitive deficits in human. Here, we assessed the importanceof Ach in Caenorhabditis elegans development, focusing onthe role of Ach during dauer formation. We found that dauerformation was disturbed in choline acetyltransferase (cha-1)and acetylcholinesterase (ace) mutants defective in Achbiosynthesis and degradation, respectively. When examinedthe potential role of G-proteins in dauer formation, goa-1 andegl-30 mutant worms, expressing mutated versions ofmammalian Go and Gq homolog, respectively, showed someabnormalities in dauer formation. Using quantitative massspectrometry, we also found that dauer larvae had lower Achcontent than did reproductively grown larvae. In addition, aproteomic analysis of acetylcholinesterase mutant worms,which have excessive levels of Ach, showed differentialexpression of metabolic genes. Collectively, these resultsindicate that alterations in Ach release may influence dauerformation in C. elegans.
참고문헌 (33)
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