Trent C et al. (1981) International C. elegans Meeting "mutants that affect egg-laying in C elegans."

Horvitz HR, Trent C, Tsung N

[International C. elegans Meeting, 1981]

Horvitz HR et al. (1979) Worm Breeder's Gazette "the serotonergic NSMs are not required for egg-laying by C elegans."

Horvitz HR, Sulston JE

[Worm Breeder's Gazette, 1979]

Horvitz HR et al. (1979) Worm Breeder's Gazette "egg-laying by C elegans as a model behavioural system."

Sulston JE, Horvitz HR, White JG

[Worm Breeder's Gazette, 1979]

Ringstad N et al. (2008) Nat Neurosci "FMRFamide neuropeptides and acetylcholine synergistically inhibit egg-laying by C. elegans."

Ringstad N, Horvitz HR

[Nat Neurosci, 2008]

Egg-laying behavior of the Caenorhabditis elegans hermaphrodite is regulated by G protein signaling pathways. Here we show that the egg laying-defective mutant egl-6(n592) carries an activating mutation in a G protein-coupled receptor that inhibits C. elegans egg-laying motor neurons in a G(o)-dependent manner. Ligands for EGL-6 are Phe-Met-Arg-Phe-NH(2) (FMRFamide)-related peptides encoded by the genes flp-10 and flp-17. flp-10 is expressed in both neurons and non-neuronal cells. The major source of flp-17 peptides is a pair of presumptive sensory neurons, the BAG neurons. Genetic analysis of the egl-6 pathway revealed that the EGL-6 neuropeptide signaling pathway functions redundantly with acetylcholine to inhibit egg-laying. The retention of embryos in the uterus of the C. elegans hermaphrodite is therefore under the control of a presumptive sensory system and is inhibited by the convergence of signals from neuropeptides and the small-molecule neurotransmitter acetylcholine.

Trent C et al. (1982) Worm Breeder's Gazette "map positions of genes that affect egg-laying in C elegans."

Horvitz HR, Tsung N, Trent C

[Worm Breeder's Gazette, 1982]

Mapping and complementation studies of egg-laying defective (egl) mutants have defined 34 new genes. These mutants are fertile, but show abnormalities in the time of onset or rate of egg-laying. Some of the mutants lay only late-stage eggs or larvae, becoming transiently bloated but eventually releasing most of their progeny. Others lay few or no eggs and become bags of worms in which progeny have hatched internally. The approximate map position of each new gene is indicated below. Mutants indicated by an allele number may be alleles of nearby egl or previously identified genes. [See Figure 1]

Weinshenker DZ et al. (1995) J Neurosci "Genetic and pharmacological analysis of neurotransmitters controlling egg laying in C. elegans."

Thomas JH, Garriga G, Weinshenker DZ

[J Neurosci, 1995]

We have investigated the neurotransmitters used to control egg-laying in C. elegans. Previous studies suggested that 5-HT released by the HSN motor neurons stimulates egg laying, and that tricyclic antidepressants potentiate egg laying by blocking reuptake of 5-HT by the HSN neurons. We report studies of the wild type and a mutant that lacks detectable 5-HT that suggest 5-HT is not required for egg-laying. Furthermore, we find that ACh is required for egg laying in response to 5-HT, suggesting that 5-HT is not sufficient to activate egg laying. The dominant egl-2(n693) mutation, which causes animals to lay eggs in response to tricyclics but not 5-HT, also conflicts with the model for egg laying. Experiments in which the HSN neurons or 5-HT are removed from egl-2 animals indicate that the action of tricyclics cannot be explained by a block of 5-HT reuptake. We find that D-2 family dopamine antagonists can also induce egg laying in egl-2(n693) mutants, and that dopamine inhibits egg laying in the wild type. These results suggest that dominant egl-2 mutations activate an inhibitory dopaminergic pathway that can be blocked by tricyclics and D-2 antagonists. We also find that these drugs stimulate egg laying in mutants lacking 5-HT or the HSN neurons, consistent with a target on the egg-laying muscles. In contrast to tricyclics, fluoxetine and other selective 5-HT reuptake inhibitors appear to be specific for 5-HT reuptake in C. elegans egg laying.

Marie L McGovern et al. (2005) International Worm Meeting "EGL-32 Functions in Sperm to Regulate Egg-laying in C. elegans"

Ling Yu, Marie L McGovern, Cathy Savage-Dunn

[International Worm Meeting, 2005]

We have uncovered a signal in sperm that regulates egg-laying in C.elegans. Hermaphrodites integrate many internal and external cues in deciding whether or not to actively lay eggs. One well known external cue is determining the presence or absence of food. We have discovered an internal cue, the presence of sperm, which is also involved in egg-laying. C.elegans are either hermaphroditic or males. The hermaphrodites do not produce sperm and oocytes at the same time. In a hermaphrodite sperm are exclusively produced during the fourth larval stage. When the worms undergo their final molt to become adults they switch to producing exclusively oocytes and will do so for the remainder of their life. Males produce exclusively sperm for their entire lives. Mutant egl-32 hermaphrodites retain about twice as many eggs as wild-type hermaphrodites. When wild-type sperm is introduced into mutant egl-32 hermaphrodites via mating, the worms begin to retain fewer eggs. When the inverse experiment is performed egl-32 males mated with wild-type hermaphrodite), the wild-type hermaphrodites begin to retain more eggs. These results suggest that sperm regulate egg-laying in C.elegans.

Tamiya H et al. (2013) J Recept Signal Transduct Res "Conserved SAMS function in regulating egg-laying in C. elegans."

Kaneko Y, Hirota K, Ishii N, Daitoku H, Iizuka K, Takahashi Y, Tamiya H, Fukamizu A, Sakuta G, Watanabe S

[J Recept Signal Transduct Res, 2013]

S-adenosyl-L-methionine (SAM) is an intermediate metabolite of methionine and serves as the methyl donor for many biological methylation reactions. The synthesis of SAM is catalyzed by SAM synthetase (SAMS), which transfers the adenosyl moiety of adenosine-5'-triphosphate to methionine. In the nematode Caenorhabditis elegans, four sams family genes, sams-1, -3, -4 and -5, are predicted to encode SAMS proteins. However, their physiological roles remain unclear. Here we show that the four predicted SAMS proteins in fact have the ability to catalyze the formation of SAM in vitro, and revealed that only sams-1 mutant animals among the family genes exhibited a significant reduction in egg-laying. Using transgenic animals carrying a transcriptional reporter for each sams gene promoter, we observed that each sams promoter confers a distinct expression pattern with respect to tissue, time of expression and expression level (i.e. promoter specificity). Promoter-swap experiments revealed that the ectopic expression of SAMS-3, -4 or -5 driven by the sams-1 promoter completely rescued egg-laying in sams-1 mutants. These data indicate that SAMS protein function is conserved throughout the entire family.

Trent C et al. (1983) International C. elegans Meeting "egg-laying defective mutants of C elegans."

Trent C, Tsung N, Horvitz HR, Desai C

[International C. elegans Meeting, 1983]

Tian, C. et al. (2009) International Worm Meeting "SEM-2 is an SRY-box transcription factor required for egg laying in C. elegans."

Stern, M., Shi, H., Tian, C., Liu, J., Colledge, C., Waterston, R.

[International Worm Meeting, 2009]

C. elegans egg laying system includes the vulva, the gonad, the hermaphrodite specific neurons and the egg-laying muscles. sem-2(n1343) mutant animals lack all the egg-laying vulval and uterine muscles (collectively called sex muscles) and are therefore egg-laying defective. The sex muscles are derived from two sex myoblasts (SMs), which are descendants of the M cell, the progenitor of the postembryonic mesodermal lineage. The absence of the sex muscles in n1343 mutants is due to a fate transformation of the SMs to their sister cells, the bodywall muscles (BWMs). We have found that sem-2(n1343) is a mutation in sox-1(C32E12.5) based on results from cosmid rescue and RNAi knockdown experiments. Furthermore, the n1343 allele contains a TC1 transposon insertion in the first 4.5kb intron of sem-2. In order to determine how sem-2 functions in regulating the SM/BWM fate decision, we examined sem-2 expression using a functional GFP::SEM-2 fusion construct. SEM-2::GFP is present in the nuclei of the SM mother cells (M. vlpa and M. vrpa), SM cells and their descendants as well as a variety of other cell types, including hypodermal cells and gut cells. By performing genetic and molecular epistasis experiments, we found that sem-2 expression in the M lineage is under the control of both dorsal-ventral and anterior-posterior patterning mechanisms that include the LIN-12/Notch pathway, the SMA-9/TGF-beta pathway and the Wnt/beta-catenin asymmetry pathway. We further found that the expression of sem-2 in the M lineage requires a conserved Hox/PBC binding site in its first intron and that this site is disrupted by the TC1 insertion in n1343 mutants. Previous studies have shown that the Hox factors MAB-5 and LIN-39 and the PBC Hox cofactor CEH-20 all function in the M lineage. We are currently testing the hypothesis that sem-2 is a direct target of Hox/PBC in the M lineage.