Abstract
eIF4E plays a conserved role in initiating protein synthesis, but with multiple eIF4E isoforms present in many organisms, these proteins also adopt specialized functions. Previous RNAi studies showed that ife-3, encoding the sole canonical eIF4E isoform of Caenorhabditis elegans, is essential for viability. Using ife-3 gene mutations, we show here that it is maternal ife-3 function that is essential for embryogenesis, but ife-3 null progeny of heterozygous animals are viable. We find that zygotic ife-3 function promotes body growth and regulates germline development in hermaphrodite worms. Specifically, the normal transition from spermatogenesis to oogenesis in the hermaphrodite germline fails in ife-3 mutants. This failure to switch is reversed by inhibiting expression of the key masculinizing gene, fem-3, suggesting ife-3 resembles a growing number of genes that promote the sperm/oocyte switch by acting genetically as upstream inhibitors of fem-3.
| Original language | English |
|---|---|
| Pages (from-to) | 843-851 |
| Number of pages | 9 |
| Journal | Biology Open |
| Volume | 4 |
| Issue number | 7 |
| DOIs | |
| State | Published - Jul 15 2015 |
Keywords
- C. Elegans
- EIF4E
- Germline
- Oogenesis
- Sex-determination
- Spermatogenesis
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