Loss of the fatty acid β-oxidation gene acaa-2 impairs timely hatching under poor maternal diet in C. elegans
Komachiya, Y.; Kato, R.; Ohno, H.
Show abstract
Developmental programs must remain robust despite fluctuations in maternal nutrition, yet the genetic basis of this robustness is incompletely understood. Using an unbiased, diet-dependent forward genetic screen in the nematode Caenorhabditis elegans, we searched for mutants with normal embryogenesis on standard food but defective development when mothers experienced poor nutrition. We isolated a mutation in acaa-2, which encodes an enzyme catalyzing the final step of mitochondrial fatty acid {beta}-oxidation, and confirmed its role using an independent deletion allele. acaa-2 mutant embryos exhibit a marked hatching delay specifically when mothers consume a low-quality diet. Despite remaining motile within the eggshell, mutant embryos are associated with increased unoccupied intra-eggshell space, consistent with impaired late embryonic growth. Our findings reveal a previously unrecognized role for acaa-2 and suggest that mitochondrial fatty acid {beta}-oxidation acts as a metabolic buffer that promotes developmental robustness under maternal nutrient limitation.
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