Caenorhabditis elegans FOS-1 and JUN-1 Regulateplc-1Expression in the Spermatheca to Control Ovulation

Abstract

Fos and Jun are components of activator protein-1 (AP-1) and play crucial roles in the regulation of many cellular, developmental, and physiological processes. Caenorhabditis elegans fos-1 has been shown to act in uterine and vulval development. Here, we provide evidence that C. elegans fos-1 and jun-1 control ovulation, a tightly regulated rhythmic program in animals. Knockdown of fos-1 or jun-1 blocks dilation of the distal spermathecal valve, a critical step for the entry of mature oocytes into the spermatheca for fertilization. Furthermore, fos-1 and jun-1 regulate the spermathecalspecific expression of plc-1, a gene that encodes a phospholipase C (PLC) isozyme that is rate-limiting for inositol triphosphate production and ovulation, and overexpression of PLC-1 rescues the ovulation defect in fos-1(RNAi) worms. Unlike fos-1, regulation of ovulation by jun-1 requires genetic interactions with eri-1 and lin-15B, which are involved in the RNA interference pathway and chromatin remodeling, respectively. At least two isoforms of jun-1 are coexpressed with fos-1b in the spermatheca, and different AP-1 dimers formed between these isoforms have distinct effects on the activation of a reporter gene. These findings uncover a novel role for FOS-1 and JUN-1 in the reproductive system and establish C. elegans as a model for studying AP-1 dimerization.

FLN-1/Filamin is required for maintenance of actin and exit of fertilized oocytes from the spermatheca in C. elegans

“…To determine if depletion of filamin in the germline can account for the observed brood size defect we used the rrf-1(pk1417) mutant strain, which is defective for somatic RNAi, but has an apparently normal germline RNAi response (Sijen et al, 2001). The rrf-1(pk1417) animals have been used previously to demonstrate a somatic role for fos-1 in the spermatheca (Hiatt et al, 2009). We found that rrf-1(pk1417) mutants treated with fln-1 RNAi did not show a significantly different brood size (270.3 ± 45.1, n=8) from control RNAi treated rrf-1(pk1417) animals (307.2 ± 28.1, n=6; Student’s t-test, p=0.1).…”

“…The plc-1(rx1) putative null animals phenocopy the exit defect of fln-1(tm545) animals, and retain multiple embryos in the spermatheca. PLC-1 is broadly expressed, and has been shown to have a role in embryogenesis, in addition to its role during ovulation (Hiatt et al, 2009; Vazquez-Manrique et al, 2008). We hypothesized that, if stretching induced by accumulated embryos causes the actin to be redistributed to the cell boundaries, the actin cytoskeleton in plc-1(rx1) spermathecal cells might be similarly disrupted.…”

Npas4: Linking Neuronal Activity to Memory

“…The table below lists some well-known IEGs expressed in the nervous system. Most IEGs found in mammals are conserved across many species, from invertebrates such as C. elegans [53], Aplysia [54] and Drosophila [55] to vertebrates, but only a subset have been tested to see whether they are rapidly induced by neuronal activity.…”

Control of Oocyte Growth and Meiotic Maturation in Caenorhabditis elegans

“…Indeed, mutations in plc-1 or plc-1(RNAi) cause spermathecal entry and exit defects (Kariya et al 2004; Yin et al 2004). PLC-1 expression in the spermatheca requires the FOS-1/JUN-1 heterodimeric transcriptional activator (Hiatt et al 2009). RNAi of fos-1 or jun-1 disrupts ovulation and this defect is rescued by expression of PLC-1 in the spermatheca (Hiatt et al 2009).…”