Loss of the fatty acid β-oxidation gene acaa-2 impairs timely hatching under poor maternal diet in C. elegans
Year: 2026
Type: preprint
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 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.
Authors: Yuzuha Komachiya, Riho Kato, Hayao Ohno
Institution: Japan Women's University
Language: English
Subfield: Aging
Domain: Life Sciences
SDG: Zero hunger
Open Access status: green
Funder: National Institutes of Health
OpenAlex ID: W7214944460