The sperm-oocyte switch in the C. elegans hermaphrodite is controlled through steady-state levels of the fem-3 mRNA

Abstract

Post-transcriptional control regulates many aspects of germline development in the Caenorhabditis elegans hermaphrodite. This nematode switches from spermatogenesis to oogenesis and is, therefore, capable of self-fertilization. This sperm-oocyte switch requires 39 UTR-mediated repression of the fem-3 mRNA. Loss of fem-3 repression results in continuous spermatogenesis in hermaphrodites. Although several factors regulating fem-3 have been identified, little is known about the mechanisms that control fem-3. Here, we investigate the steady-state levels of the fem-3 transcript and the expression pattern of its protein product. We show that FEM-3 is exclusively present in germ cells that are committed to spermatogenesis. We found that in fem-3(gf)/+ heterozygotes, mutant fem-3 gain-of-function transcripts are more abundant than their wild-type counterpart. Furthermore, we show that the penetrance of the fem-3(gf) allele correlates with inefficient FBF binding and extended poly(A) tail size of fem-3 mRNAs. Finally, we show that wild-type and gain-of-function mutated fem-3 mRNAs associate equally well with polyribosomes. We propose that the fem-3 mRNA is regulated through stabilization rather than through translatability.

The Ccr4-Not deadenylase complex constitutes the major poly(A) removal activity inC. elegans

“…Even unrecognized defects in somatic cells of the gonad may be causal. Although an involvement of ccf-1 and ccr-4 in post-transcriptional regulation of mRNA-specific gene expression has been suggested in C. elegans Suh et al, 2009;Zanetti et al, 2012), it remained unclear how prevalent Ccr4-Not complexmediated deadenylation is at the global level. The combined biological and molecular results of this study argue for an evolutionarily conserved need of regulated mRNA poly(A) tail shortening in female germ cells that is provided broadly by CCF-1 of the Ccr4-Not complex, and probably fine-tuned by CCR-4 deadenylase activity.…”

The role of LARP1 in translation and beyond

“…Hemaphrodites ( larp‐1(0) ; nos‐3(q650)) lose their Mog phenotype in the fem‐3 (e2006) null context and displays 95% feminization. More significantly, loss of larp‐1 function increases the Mog phenotype of two fem‐3 gain of function mutants ( fem‐3 (q22) and fem‐3 (q23) ) . A direct assessment of fem‐3 mRNA levels in larp‐1(0) L4 hermaphrodites show a two‐ to three‐fold increase as compared to wild‐type.…”

“…After a transient period of sperm production at larval stage L3, repression of FEM‐3 protein production is required to switch to the female program (for review see Ref ). fem‐3(e2006) temperature‐sensitive loss of function hermaphrodites are almost 100% female at high temperature (25°C), while gain of function mutants show Mog phenotypes (more or less penetrant according to the allele) . CeLARP1 has been proposed to promote oogenesis through negatively regulating fem‐3 mRNA levels.…”

“…So far the roles of LARP1 proteins in whole organism development and survival have been investigated in three species: C. elegans, 32,43,44 D. melanogaster, 35,39 and A. thaliana. 41 While worm and fly LARP1 retain a crucial function in reproduction, no fertility deficiencies were observed in Arabidopsis null Atlarp1 mutant BOX 2…”

Alternative Splicing Regulation of Cancer-Related Pathways inCaenorhabditis elegans: An In Vivo Model System with a Powerful Reverse Genetics Toolbox

“…During its development, the hermaphrodite worms produce sperm at one stage of their life cycle before switching to produce oocytes. The molecular pathways of this sperm to oocyte transition have been studied extensively [2]. Its complete genome, sequenced in 1998, was the first sequenced genome from a multicellular organism.…”