scholarly journals Regulatory changes in two chemoreceptor genes contribute to a Caenorhabditis elegans QTL for foraging behavior

eLife ◽  
2016 ◽  
Vol 5 ◽  
Author(s):  
Joshua S Greene ◽  
May Dobosiewicz ◽  
Rebecca A Butcher ◽  
Patrick T McGrath ◽  
Cornelia I Bargmann

Natural isolates of C. elegans differ in their sensitivity to pheromones that inhibit exploratory behavior. Previous studies identified a QTL for pheromone sensitivity that includes alternative alleles of srx-43, a chemoreceptor that inhibits exploration through its activity in ASI sensory neurons. Here we show that the QTL is multigenic and includes alternative alleles of srx-44, a second chemoreceptor gene that modifies pheromone sensitivity. srx-44 either promotes or inhibits exploration depending on its expression in the ASJ or ADL sensory neurons, respectively. Naturally occurring pheromone insensitivity results in part from previously described changes in srx-43 expression levels, and in part from increased srx-44 expression in ASJ, which antagonizes ASI and ADL. Antagonism between the sensory neurons results in cellular epistasis that is reflected in their transcription of insulin genes that regulate exploration. These results and genome-wide evidence suggest that chemoreceptor genes may be preferred sites of adaptive variation in C. elegans.

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Mercedes M. Pérez-Jiménez ◽  
José M. Monje-Moreno ◽  
Ana María Brokate-Llanos ◽  
Mónica Venegas-Calerón ◽  
Alicia Sánchez-García ◽  
...  

AbstractAging and fertility are two interconnected processes. From invertebrates to mammals, absence of the germline increases longevity. Here we show that loss of function of sul-2, the Caenorhabditis elegans steroid sulfatase (STS), raises the pool of sulfated steroid hormones, increases longevity and ameliorates protein aggregation diseases. This increased longevity requires factors involved in germline-mediated longevity (daf-16, daf-12, kri-1, tcer-1 and daf-36 genes) although sul-2 mutations do not affect fertility. Interestingly, sul-2 is only expressed in sensory neurons, suggesting a regulation of sulfated hormones state by environmental cues. Treatment with the specific STS inhibitor STX64, as well as with testosterone-derived sulfated hormones reproduces the longevity phenotype of sul-2 mutants. Remarkably, those treatments ameliorate protein aggregation diseases in C. elegans, and STX64 also Alzheimer’s disease in a mammalian model. These results open the possibility of reallocating steroid sulfatase inhibitors or derivates for the treatment of aging and aging related diseases.


Author(s):  
Gaotian Zhang ◽  
Jake D Mostad ◽  
Erik C Andersen

Abstract Life history traits underlie the fitness of organisms and are under strong natural selection. A new mutation that positively impacts a life history trait will likely increase in frequency and become fixed in a population (e.g. a selective sweep). The identification of the beneficial alleles that underlie selective sweeps provides insights into the mechanisms that occurred during the evolution of a species. In the global population of Caenorhabditis elegans, we previously identified selective sweeps that have drastically reduced chromosomal-scale genetic diversity in the species. Here, we measured the fecundity of 121 wild C. elegans strains, including many recently isolated divergent strains from the Hawaiian islands and found that strains with larger swept genomic regions have significantly higher fecundity than strains without evidence of the recent selective sweeps. We used genome-wide association (GWA) mapping to identify three quantitative trait loci (QTL) underlying the fecundity variation. Additionally, we mapped previous fecundity data from wild C. elegans strains and C. elegans recombinant inbred advanced intercross lines that were grown in various conditions and detected eight QTL using GWA and linkage mappings. These QTL show the genetic complexity of fecundity across this species. Moreover, the haplotype structure in each GWA QTL region revealed correlations with recent selective sweeps in the C. elegans population. North American and European strains had significantly higher fecundity than most strains from Hawaii, a hypothesized origin of the C. elegans species, suggesting that beneficial alleles that caused increased fecundity could underlie the selective sweeps during the worldwide expansion of C. elegans.


Lab on a Chip ◽  
2017 ◽  
Vol 17 (10) ◽  
pp. 1725-1731 ◽  
Author(s):  
Wei Zhou ◽  
Jingjing Wang ◽  
Kaiyue Wang ◽  
Bin Huang ◽  
Lili Niu ◽  
...  

We demonstrate an ultrasound neuro-modulation chip capable of activating neurons of the C. elegans directly.


2020 ◽  
Author(s):  
Yukihiro Kubota ◽  
Yuto Ohnishi ◽  
Tasuku Hamasaki ◽  
Gen Yasui ◽  
Natsumi Ota ◽  
...  

AbstractHistone deacetylases (HDACs) are divided into four classes. Class-I HDAC, HDAC-1 forms three types of complexes, namely the Nucleosome Remodeling Deacetylase complex, the Sin3 complex, and the CoREST complex, with specific corepressor component Mi2/CHD-3, Sin3, and RCOR1 in human, respectively. The functions of these HDAC-1 complexes are regulated by their corepressors, however, their exact mechanistic roles in several biological processes remain unexplored, such as in embryonic development. Here, we report that each of the corepressors, LET-418, SIN-3, and SPR-1, the homologous of Mi2, Sin3, and RCOR1, respectively, were expressed throughout Caenorhabditis elegans embryonic development and served essential roles in the process. Moreover, genetic analysis suggested that three pathways (i.e., LET-418– SIN-3–SPR-1, SIN-3–SPR-1, and LET-418) participated in embryonic development. Our terminal-phenotype observations of single mutants of each corepressor implied that LET-418, SIN-3, and SPR-1 played similar roles in promoting advancement to the middle and late embryonic stages. Genome-wide comparative-transcriptome analysis indicated that 47.5% and 42.3% of genes were commonly increased and decreased in sin-3 and spr-1 mutants, respectively. These results suggest that among the three pathways studied, the SIN-3–SPR-1 pathway mainly serves to regulate embryonic development. Comparative-Gene Ontology analysis indicated that these three pathways played overlapping and distinct roles in regulating C. elegans embryonic development.


2016 ◽  
Author(s):  
Joshua S Greene ◽  
May Dobosiewicz ◽  
Rebecca A Butcher ◽  
Patrick T McGrath ◽  
Cornelia I Bargmann

Genetics ◽  
2020 ◽  
Vol 216 (1) ◽  
pp. 145-157
Author(s):  
Tiffany Baiocchi ◽  
Kyle Anesko ◽  
Nathan Mercado ◽  
Heenam Park ◽  
Kassandra Kin ◽  
...  

Chemosensation plays a role in the behaviors and life cycles of numerous organisms, including nematodes. Many guilds of nematodes exist, ranging from the free-living Caenorhabditis elegans to various parasitic species such as entomopathogenic nematodes (EPNs), which are parasites of insects. Despite ecological differences, previous research has shown that both EPNs and C. elegans respond to prenol (3-methyl-2-buten-1-ol), an odor associated with EPN infections. However, it is unclear how C. elegans responds to prenol. By utilizing natural variation and genetic neuron ablation to investigate the response of C. elegans to prenol, we found that the AWC neurons are involved in the detection of prenol and that several genes (including dcap-1, dcap-2, and clec-39) influence response to this odorant. Furthermore, we identified that the response to prenol is mediated by the canonically proposed pathway required for other AWC-sensed attractants. However, upon testing genetically diverse isolates, we found that the response of some strains to prenol differed from their response to isoamyl alcohol, suggesting that the pathways mediating response to these two odorants may be genetically distinct. Further, evaluations leveraging natural variation and genome wide association revealed specific genes that influence nematode behavior and provide a foundation for future studies to better understand the role of prenol in nematode behavioral ecology.


2000 ◽  
Vol 113 (21) ◽  
pp. 3825-3837 ◽  
Author(s):  
T.Q. Nguyen ◽  
H. Sawa ◽  
H. Okano ◽  
J.G. White

Septins have been shown to play important roles in cytokinesis in diverse organisms ranging from yeast to mammals. In this study, we show that both the unc-59 and unc-61 loci encode Caenorhabditis elegans septins. Genomic database searches indicate that unc-59 and unc-61 are probably the only septin genes in the C. elegans genome. UNC-59 and UNC-61 localize to the leading edge of cleavage furrows and eventually reside at the midbody. Analysis of unc-59 and unc-61 mutants revealed that each septin requires the presence of the other for localization to the cytokinetic furrow. Surprisingly, unc-59 and unc-61 mutants generally have normal embryonic development; however, defects were observed in post-embryonic development affecting the morphogenesis of the vulva, male tail, gonad, and sensory neurons. These defects can be at least partially attributed to failures in post-embryonic cytokineses although our data also suggest other possible roles for septins. unc-59 and unc-61 double mutants show similar defects to each of the single mutants.


2014 ◽  
Vol 83 (1) ◽  
pp. 17-27 ◽  
Author(s):  
George W. P. Joshua ◽  
Steve Atkinson ◽  
Robert J. Goldstone ◽  
Hannah L. Patrick ◽  
Richard A. Stabler ◽  
...  

The formation of an incapacitating biofilm onCaenorhabditis elegansbyYersinia pseudotuberculosisrepresents a tractable model for investigating the genetic basis for host-pathogen interplay during the biofilm-mediated infection of a living surface. Previously we established a role for quorum sensing (QS) and the master motility regulator, FlhDC, in biofilm formation byY. pseudotuberculosisonC. elegans. To obtain further genome-wide insights, we used transcriptomic analysis to obtain comparative information onC. elegansin the presence and absence of biofilm and on wild-typeY. pseudotuberculosisandY. pseudotuberculosisQS mutants. Infection ofC. eleganswith the wild-typeY. pseudotuberculosisresulted in the differential regulation of numerous genes, including a distinct subset of nematode C-lectin (clec) and fatty acid desaturase (fat) genes. Evaluation of the correspondingC. elegansclec-49andfat-3deletion mutants showed delayed biofilm formation and abolished biofilm formation, respectively. Transcriptomic analysis ofY. pseudotuberculosisrevealed that genes located in both of the histidine utilization (hut) operons were upregulated in both QS andflhDCmutants. In addition, mutation of the regulatory genehutCresulted in the loss of biofilm, increased expression offlhDC, and enhanced swimming motility. These data are consistent with the existence of a regulatory cascade in which the Hut pathway links QS andflhDC. This work also indicates that biofilm formation byY. pseudotuberculosisonC. elegansis an interactive process during which the initial attachment/recognition ofYersiniato/byC. elegansis followed by bacterial growth and biofilm formation.


Genetics ◽  
2003 ◽  
Vol 164 (1) ◽  
pp. 127-134
Author(s):  
Sylvia E J Fischer ◽  
Erno Wienholds ◽  
Ronald H A Plasterk

Abstract In a genome-wide analysis of the active transposons in Caenorhabditis elegans we determined the localization and sequence of all copies of each of the six active transposon families. Most copies of the most active transposons, Tc1 and Tc3, are intact but individually have a unique sequence, because of unique patterns of single-nucleotide polymorphisms. The sequence of each of the 32 Tc1 elements is invariant in the C. elegans strain N2, which has no germline transposition. However, at the same 32 Tc1 loci in strains with germline transposition, Tc1 elements can acquire the sequence of Tc1 elements elsewhere in the N2 genome or a chimeric sequence derived from two dispersed Tc1 elements. We hypothesize that during double-strand-break repair after Tc1 excision, the template for repair can switch from the Tc1 element on the sister chromatid or homologous chromosome to a Tc1 copy elsewhere in the genome. Thus, the population of active transposable elements in C. elegans is highly dynamic because of a continuous exchange of sequence information between individual copies, potentially allowing a higher evolution rate than that found in endogenous genes.


2004 ◽  
Vol 26 (5) ◽  
pp. 25-28
Author(s):  
Gino Poulin ◽  
David P. Welchman

RNAi-mediated silencing is now being used in multiple species, from plants to humans, to identify gene functions. This new technology is fully exploited in Caenorhabditis elegans, since an RNAi feeding library that has the potential to inactivate 86% of the predicted genes of the C. elegans genome is publicly available. This tool made systematic screening of genes involved in biological processes of interest easier, but there are some pitfalls: specificity, reproducibility and hypomorphic effects. However, as with any other technology, RNAi is getting better as time goes on. Once these caveats are taken into account, RNAi-mediated silencing is still a very powerful approach to identify new gene functions and to dissect complex pathways.


Sign in / Sign up

Export Citation Format

Share Document