Mangio Richard S, Votra SarahBeth, Pruyne David
Department of Biochemistry and Molecular Biology, SUNY Upstate Medical University, Syracuse, NY 13210, USA.
Department of Cell and Developmental Biology, SUNY Upstate Medical University, Syracuse, NY 13210, USA.
Biol Open. 2015 May 15;4(7):843-51. doi: 10.1242/bio.011585.
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.
真核细胞起始因子4E（eIF4E）在启动蛋白质合成过程中发挥着保守作用，但由于许多生物体中存在多种eIF4E异构体，这些蛋白质也具有特殊功能。先前的RNA干扰研究表明，编码秀丽隐杆线虫唯一标准eIF4E异构体的ife-3对其生存能力至关重要。通过使用ife-3基因突变，我们在此表明，母体ife-3功能对胚胎发生至关重要，但杂合动物的ife-3缺失后代是可存活的。我们发现，合子ife-3功能促进雌雄同体蠕虫的身体生长并调节生殖系发育。具体而言，雌雄同体生殖系中从精子发生到卵子发生的正常转变在ife-3突变体中失败。通过抑制关键的雄性化基因fem-3的表达可以逆转这种转变失败，这表明ife-3类似于越来越多的基因，这些基因通过在遗传上作为fem-3的上游抑制剂来促进精子/卵子的转变。
