Loss of the fatty acid β‑oxidation gene acaa‑2 impairs timely hatching under poor maternal diet in C. elegans

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 β-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 β-oxidation acts as a metabolic buffer that promotes developmental robustness under maternal nutrient limitation.