Answers are grounded in this paper and cite their sources.
Research uncovers specific requirements for C. elegans notch ligand APX-1 in embryonic viability and fertility, indicating complex interactions involved.
Requirements for the C. elegans Notch ligand APX-1 have been described, but the molecular lesions in mutant alleles remain unknown. Here we report the sequence changes in three previously isolated non-conditional alleles and two newly isolated alleles, apx-1(or545ts) and a null allele apx-1(or2015). All alleles resulted in highly penetrant embryonic lethality but only null mutations greatly reduced brood sizes. This reproductive phenotype was likely due to abnormal ovulation rupturing oocytes and, together with vulva defects, resulting in debris accumulation that prevented embryo passage. In addition to identifying molecular lesions in apx-1 alleles and clarifying distinct requirements for C. elegans Notch ligands, our results reveal extensive genotype-by-environment interactions, including haploinsufficiency of essential loci at a stressfully high growth temperature, and highlight the origins of complex phenotypes as a consequence of multiple seemingly unrelated defects.
No takes yet. Share an insight, caveat, or question.
Chuang et al. (2025) studied this question.
Synapse has enriched 10 related papers. Consider them for comparative context: