Journal
G3-GENES GENOMES GENETICS
Volume 9, Issue 3, Pages 901-909Publisher
GENETICS SOCIETY AMERICA
DOI: 10.1534/g3.118.200863
Keywords
sex determination; microRNAs; embryogenesis; XO lethality; germline sex determination; Genetics of Sex
Categories
Funding
- NIDDK Intramural Research Program [1ZII DK075147-01]
- NIH Office of Research Infrastructure Programs [P40 OD010440]
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The germline sex determination pathway in C. elegans determines whether germ cells develop as oocytes or sperm, with no previously known effect on viability. The family of microRNAs are expressed in the C. elegans germline and embryo and are essential for both viability and normal hermaphroditic sex determination, preventing aberrant male gene expression in XX hermaphrodite embryos. Here we show that combining feminizing mutations with partial loss of function of the family results in enhanced penetrance embryonic lethality that preferentially kills XO animals. This lethal phenotype is due to altered signaling through the germline sex determination pathway, and maternal germline feminization is sufficient to induce enhanced lethality. These findings reveal a surprising pleiotropy of sperm-fate promoting pathways on organismal viability. Overall, our results demonstrate an unexpectedly strong link between sex determination and embryonic viability, and suggest that in wild type animals, family members buffer against misregulation of pathways outside the sex determination program, allowing for clean sex reversal rather than deleterious effects of perturbing sex determination genes.
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