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

2009 ◽  
Vol 20 (17) ◽  
pp. 3888-3895 ◽  
Author(s):  
Susan M. Hiatt ◽  
Holli M. Duren ◽  
Y. John Shyu ◽  
Ronald E. Ellis ◽  
Naoki Hisamoto ◽  
...  
Keyword(s):  
Caenorhabditis Elegans ◽  
Chromatin Remodeling ◽  
Genetic Interactions ◽  
Inositol Triphosphate ◽  
Activator Protein 1 ◽  
Specific Expression ◽  
Vulval Development ◽  
C Elegans ◽  
Physiological Processes ◽  
Rate Limiting

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 spermathecal-specific 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.

scholarly journals An economical and highly adaptable optogenetics system for individual and population-level manipulation of Caenorhabditis elegans

BMC Biology ◽  
2021 ◽  
Vol 19 (1) ◽  
Author(s):  
M. Koopman ◽  
L. Janssen ◽  
E. A. A. Nollen
Keyword(s):  
Caenorhabditis Elegans ◽  
Light Stimulus ◽  
Cholinergic Neurons ◽  
Model Organisms ◽  
Parameter Study ◽  
Multiple Model ◽  
Excitable Cells ◽  
Specific Expression ◽  
C Elegans ◽  
Age Related

Abstract Background Optogenetics allows the experimental manipulation of excitable cells by a light stimulus without the need for technically challenging and invasive procedures. The high degree of spatial, temporal, and intensity control that can be achieved with a light stimulus, combined with cell type-specific expression of light-sensitive ion channels, enables highly specific and precise stimulation of excitable cells. Optogenetic tools have therefore revolutionized the study of neuronal circuits in a number of models, including Caenorhabditis elegans. Despite the existence of several optogenetic systems that allow spatial and temporal photoactivation of light-sensitive actuators in C. elegans, their high costs and low flexibility have limited wide access to optogenetics. Here, we developed an inexpensive, easy-to-build, modular, and adjustable optogenetics device for use on different microscopes and worm trackers, which we called the OptoArm. Results The OptoArm allows for single- and multiple-worm illumination and is adaptable in terms of light intensity, lighting profiles, and light color. We demonstrate OptoArm’s power in a population-based multi-parameter study on the contributions of motor circuit cells to age-related motility decline. We found that individual components of the neuromuscular system display different rates of age-dependent deterioration. The functional decline of cholinergic neurons mirrors motor decline, while GABAergic neurons and muscle cells are relatively age-resilient, suggesting that rate-limiting cells exist and determine neuronal circuit ageing. Conclusion We have assembled an economical, reliable, and highly adaptable optogenetics system which can be deployed to address diverse biological questions. We provide a detailed description of the construction as well as technical and biological validation of our set-up. Importantly, use of the OptoArm is not limited to C. elegans and may benefit studies in multiple model organisms, making optogenetics more accessible to the broader research community.

scholarly journals Feeding recombinant Royalactin: Measures of improved lifespan and mitochondrial function in Caenorhabditis elegans

2020 ◽  
Author(s):  
Xia Li ◽  
Thomas L. Ingram ◽  
Ying Wang ◽  
Kamila Derecka ◽  
Nathan Courtier ◽  
...  
Keyword(s):  
Caenorhabditis Elegans ◽  
Mitochondrial Function ◽  
Royal Jelly ◽  
Biological Functions ◽  
C Elegans ◽  
Beneficial Effects ◽  
Physiological Processes ◽  
Royal Jelly Protein ◽  
Insight Into ◽  
Over Time

AbstractAgeing, the decline of biological functions over time, is inherent to eukaryotes. Female honeybees attain a long-lived queen phenotype upon continuous consumption of royal jelly, whereas restricted supply of this nutritional substance promotes the development of worker bees, which are short-lived. An abundant protein found within royal jelly is major royal jelly protein 1 (MRJP1), also known as ‘Royalactin’. Health- and lifespan promoting effects have been attributed to Royalactin in species from diverse animal taxa, suggesting it acts on phylogenetically conserved physiological processes. Here, we explore the effects of feeding the nematode Caenorhabditis elegans with Escherichia coli that express a recombinant form of Royalactin (RArec). We confirm that consumption of RArec increases body size, improves locomotion and extends lifespan. We discover a link between Royalactin and mitochondria, organelles which play a key part in the ageing process: both spare respiratory capacity and morphology indicate improved mitochondrial function in RArec fed C. elegans. These results demonstrate the feasibility of using recombinant Royalactin to gain further insight into processes of healthy ageing in many species.RArec production allows insight into potential beneficial effects across species.

Uncover Genetic Interactions in Caenorhabditis elegans by RNA Interference

2005 ◽  
Vol 25 (5-6) ◽  
pp. 299-307 ◽  
Author(s):  
Angelo Fortunato ◽  
Andrew G. Fraser
Keyword(s):  
Rna Interference ◽  
Caenorhabditis Elegans ◽  
Gene Function ◽  
Genetic Interactions ◽  
Loss Of Function ◽  
Future Directions ◽  
C Elegans ◽  
Genomics Tools ◽  
Almost All ◽  
Nematode Worm

RNA-mediated interference (RNAi) has emerged recently as one of the most powerful functional genomics tools. RNAi has been particularly effective in the nematode worm C. elegans where RNAi has been used to analyse the loss-of-function phenotypes of almost all predicted genes. In this review, we illustrate how RNAi has been used to analyse gene function in C. elegans as well as pointing to some future directions for using RNAi to examine genetic interactions in a systematic manner.

scholarly journals Synthetic Lethal Genetic Interactions That Decrease Somatic Cell Proliferation in Caenorhabditis elegans Identify the Alternative RFCCTF18 as a Candidate Cancer Drug Target

2009 ◽  
Vol 20 (24) ◽  
pp. 5306-5313 ◽  
Author(s):  
Jessica McLellan ◽  
Nigel O'Neil ◽  
Sanja Tarailo ◽  
Jan Stoepel ◽  
Jennifer Bryan ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Caenorhabditis Elegans ◽  
Somatic Cell ◽  
Therapeutic Targets ◽  
Genetic Interactions ◽  
Assay System ◽  
Cancer Drug ◽  
Mild Phenotype ◽  
Synthetic Lethal ◽  
C Elegans

Somatic mutations causing chromosome instability (CIN) in tumors can be exploited for selective killing of cancer cells by knockdown of second-site genes causing synthetic lethality. We tested and statistically validated synthetic lethal (SL) interactions between mutations in six Saccharomyces cerevisiae CIN genes orthologous to genes mutated in colon tumors and five additional CIN genes. To identify which SL interactions are conserved in higher organisms and represent potential chemotherapeutic targets, we developed an assay system in Caenorhabditis elegans to test genetic interactions causing synthetic proliferation defects in somatic cells. We made use of postembryonic RNA interference and the vulval cell lineage of C. elegans as a readout for somatic cell proliferation defects. We identified SL interactions between members of the cohesin complex and CTF4, RAD27, and components of the alternative RFCCTF18 complex. The genetic interactions tested are highly conserved between S. cerevisiae and C. elegans and suggest that the alternative RFC components DCC1, CTF8, and CTF18 are ideal therapeutic targets because of their mild phenotype when knocked down singly in C. elegans . Furthermore, the C. elegans assay system will contribute to our knowledge of genetic interactions in a multicellular animal and is a powerful approach to identify new cancer therapeutic targets.

scholarly journals Functional Requirement for Histone Deacetylase 1 in Caenorhabditis elegans Gonadogenesis

2002 ◽  
Vol 22 (9) ◽  
pp. 3024-3034 ◽  
Author(s):  
Pascale Dufourcq ◽  
Martin Victor ◽  
Frédérique Gay ◽  
Dominica Calvo ◽  
Jonathan Hodgkin ◽  
...  
Keyword(s):  
Caenorhabditis Elegans ◽  
Histone Deacetylase ◽  
Histone Deacetylases ◽  
Regulation Of Gene Expression ◽  
Notch Signaling Pathway ◽  
Transcriptional Repressors ◽  
Vulval Development ◽  
C Elegans ◽  
Histone Deacetylase 1 ◽  
Multicellular Organisms

ABSTRACT Histone acetylation and deacetylation have been implicated in the regulation of gene expression. Molecular studies have shown that histone deacetylases (HDACs) function as transcriptional repressors. However, very little is known about their roles during development in multicellular organisms. We previously demonstrated that inhibition of maternal and zygotic expression of histone deacetylase 1 (HDA-1) causes embryonic lethality in Caenorhabditis elegans. Here, we report the identification of an hda-1 genetic mutant which has also been called a gon-10 mutant (for gonadogenesis defective 10) and show that loss of HDA-1 zygotic expression results in specific postembryonic defects in gonadogenesis and vulval development. We provide evidence that the lag-2 gene, which plays a role in gonadogenesis and vulval development and encodes a Notch ligand, is derepressed in gon-10 animals, suggesting that lag-2 may be a target of HDA-1. Our findings reveal a novel and specific function for the ubiquitously expressed HDA-1 in C. elegans gonadogenesis and place hda-1 in the Notch signaling pathway.

scholarly journals Akirin Is Required for Muscle Function and Acts Through the TGF-β Sma/Mab Signaling Pathway in Caenorhabditis elegans Development

2019 ◽  
Vol 10 (1) ◽  
pp. 387-400 ◽  
Author(s):  
Richard Bowman ◽  
Nathan Balukoff ◽  
Amy Clemons ◽  
Emily Koury ◽  
Talitha Ford ◽  
...  
Keyword(s):  
Body Size ◽  
Caenorhabditis Elegans ◽  
Signaling Pathway ◽  
Chromatin Remodeling ◽  
Muscle Development ◽  
The Body ◽  
Model Systems ◽  
Loss Of Function ◽  
C Elegans ◽  
Chromatin Remodeling Complex

Akirin, a conserved metazoan protein, functions in muscle development in flies and mice. However, this was only tested in the rodent and fly model systems. Akirin was shown to act with chromatin remodeling complexes in transcription and was established as a downstream target of the NFκB pathway. Here we show a role for Caenorhabditis elegans Akirin/AKIR-1 in the muscle and body length regulation through a different pathway. Akirin localizes to somatic tissues throughout the body of C. elegans, including muscle nuclei. In agreement with its role in other model systems, Akirin loss of function mutants exhibit defects in muscle development in the embryo, as well as defects in movement and maintenance of muscle integrity in the C. elegans adult. We also have determined that Akirin acts downstream of the TGF-β Sma/Mab signaling pathway in controlling body size. Moreover, we found that the loss of Akirin resulted in an increase in autophagy markers, similar to mutants in the TGF-β Sma/Mab signaling pathway. In contrast to what is known in rodent and fly models, C. elegans Akirin does not act with the SWI/SNF chromatin-remodeling complex, and is instead involved with the NuRD chromatin remodeling complex in both movement and regulation of body size. Our studies define a novel developmental role (body size) and a new pathway (TGF-β Sma/Mab) for Akirin function, and confirmed its evolutionarily conserved function in muscle development in a new organism.

scholarly journals The Enigmatic Canal-Associated Neurons Regulate Caenorhabditis elegans Larval Development Through a cAMP Signaling Pathway

Genetics ◽  
2019 ◽  
Vol 213 (4) ◽  
pp. 1465-1478
Author(s):  
Jason Chien ◽  
Fred W. Wolf ◽  
Sarah Grosche ◽  
Nebeyu Yosef ◽  
Gian Garriga ◽  
...  
Keyword(s):  
Caenorhabditis Elegans ◽  
Adenylyl Cyclase ◽  
Larval Development ◽  
Target Cells ◽  
Specific Expression ◽  
C Elegans ◽  
Link Type ◽  
Similar Phenotype ◽  
Link Loss ◽  
Pka Pathway

Caenorhabditis elegans larval development requires the function of the two Canal-Associated Neurons (CANs): killing the CANs by laser microsurgery or disrupting their development by mutating the gene ceh-10 results in early larval arrest. How these cells promote larval development, however, remains a mystery. In screens for mutations that bypass CAN function, we identified the gene kin-29, which encodes a member of the Salt-Inducible Kinase (SIK) family and a component of a conserved pathway that regulates various C. elegans phenotypes. Like kin-29 loss, gain-of-function mutations in genes that may act upstream of kin-29 or growth in cyclic-AMP analogs bypassed ceh-10 larval arrest, suggesting that a conserved adenylyl cyclase/PKA pathway inhibits KIN-29 to promote larval development, and that loss of CAN function results in dysregulation of KIN-29 and larval arrest. The adenylyl cyclase ACY-2 mediates CAN-dependent larval development: acy-2 mutant larvae arrested development with a similar phenotype to ceh-10 mutants, and the arrest phenotype was suppressed by mutations in kin-29. ACY-2 is expressed predominantly in the CANs, and we provide evidence that the acy-2 functions in the CANs to promote larval development. By contrast, cell-specific expression experiments suggest that kin-29 acts in both the hypodermis and neurons, but not in the CANs. Based on our findings, we propose two models for how ACY-2 activity in the CANs regulates KIN-29 in target cells.

scholarly journals Overlapping and non-overlapping roles of the class-I histone deacetylase-1 corepressors LET-418, SIN-3, and SPR-1 in Caenorhabditis elegans embryonic development

2021 ◽  
Author(s):  
Yukihiro Kubota ◽  
Yuto Ohnishi ◽  
Tasuku Hamasaki ◽  
Gen Yasui ◽  
Natsumi Ota ◽  
...  
Keyword(s):  
Caenorhabditis Elegans ◽  
Embryonic Development ◽  
Histone Deacetylase ◽  
Genetic Interactions ◽  
Class I ◽  
Specific Cell ◽  
Nucleosome Remodeling ◽  
Expression Levels ◽  
C Elegans ◽  
Functional Relationships

AbstractBackgroundHistone deacetylase (HDAC)-1, a Class-I HDAC family member, forms three types of complexes, the nucleosome remodeling deacetylase, Sin3, and CoREST complexes with the specific corepressor components chromodomain-helicase-DNA-binding protein 3 (Mi2/CHD-3), Sin3, and REST corepressor 1 (RCOR1), respectively, in humans.ObjectiveTo elucidate the functional relationships among the three transcriptional corepressors during embryogenesis.MethodsThe activities of HDA-1, LET-418, SIN-3, and SPR-1, the homologs of HDAC-1, Mi2, Sin3, and RCOR1 inCaenorhabditis elegansduring embryogenesis were investigated through measurement of relative mRNA expression levels and embryonic lethality given either gene knockdown or deletion. Additionally, the terminal phenotypes of each knockdown and mutant embryo were observed using a differential-interference contrast microscope. Finally, the functional relationships among the three corepressors were examined through genetic interactions and transcriptome analyses.ResultsHere, we report that each of the corepressors LET-418, SIN-3, and SPR-1 are expressed and have essential roles inC. elegansembryonic development. Our terminal phenotype observations of single mutants further implied that LET-418, SIN-3, and SPR-1 play similar roles in promoting advancement to the middle and late embryonic stages. Combined analysis of genetic interactions and gene ontology of these corepressors indicate a prominent overlapping role among SIN-3, SPR-1, and LET-418 and between SIN-3 and SPR-1.ConclusionOur findings suggest that the class-I HDAC-1 corepressors LET-418, SIN-3, and SPR-1 may cooperatively regulate the expression levels of some genes duringC. elegansembryogenesis or may have some similar roles but functioning independently within a specific cell.

scholarly journals Mosaic Analysis Using a ncl-1 (+) Extrachromosomal Array Reveals That lin-31 Acts in the Pn.p Cells During Caenorhabditis elegans Vulval Development

Genetics ◽  
1996 ◽  
Vol 143 (3) ◽  
pp. 1181-1191 ◽  
Author(s):  
Leilani M Miller ◽  
David A Waxing ◽  
Stuart K Kim
Keyword(s):  
Caenorhabditis Elegans ◽  
The Body ◽  
Specific Cell ◽  
Vulval Development ◽  
C Elegans ◽  
Genetic Mosaic ◽  
Extrachromosomal Array ◽  
Mosaic Analysis ◽  
Putative Transcription Factor ◽  
Sites Of Action

Abstract We describe a genetic mosaic analysis procedure in which Caenorhabditis elegans mosaics are generated by spontaneous loss of an extrachromosomal array. This technique allows almost any C. elegans gene that can be used in germline transformation experiments to be used in mosaic analysis experiments. We identified a cosmid clone that rescues the mutant phenotype of ncl-1, so that this cell-autonomous marker could be used to analyze mosaic animals. To determine the sites of action for unc-29 and lin-31, an extrachromosomal array was constructed containing the ncl-1(+) cosmid linked to lin-31(+) and unc-29(+) cosmids. This array is mitotically unstable and can be lost to produce a clone of mutant cells. The specific cell division at which the extrachromosomal array had been lost was deduced by scoring the Ncl phenotypes of individual cells in genetic mosaics. The Unc-29 and Lin-31 phenotypes were then scored in these animals to determine in which cells these genes are required. This analysis showed that unc-29, which encodes a subunit of the acetylcholine receptor, acts in the body muscle cells. Furthermore, lin-31, which specifies cell fates during vulval induction and encodes a putative transcription factor similar to HNF-3/fork head, acts in the Pn.p cells

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