Loss of the fatty acid β-oxidation gene acaa-2 impairs timely hatching under poor maternal diet in C. elegans
- 1Division of Material and Biological Sciences, Graduate School of Science, Japan Women's University
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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BibTeX
@misc{komachiya2026loss,
title = {{Loss of the fatty acid β-oxidation gene acaa-2 impairs timely hatching under poor maternal diet in C. elegans}},
author = {Y. Komachiya and R. Kato and H. Ohno},
howpublished = {bioRxiv},
year = {2026},
month = sep,
doi = {10.64898/2026.09.29.755286},
url = {https://www.biorxiv.org/content/10.64898/2026.09.29.755286v1},
note = {CC BY-NC-ND},
}
RIS
TY - UNPB
TI - Loss of the fatty acid β-oxidation gene acaa-2 impairs timely hatching under poor maternal diet in C. elegans
AU - Y. Komachiya
AU - R. Kato
AU - H. Ohno
PY - 2026
DA - 2026/09/29
PB - bioRxiv
DO - 10.64898/2026.09.29.755286
UR - https://www.biorxiv.org/content/10.64898/2026.09.29.755286v1
AB - 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.
ER -