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Journal articles on the topic 'Elegans dauer'

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Published: 5 June 2025

Last updated: 15 July 2025

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Ailion, Michael, and James H. Thomas. "Dauer Formation Induced by High Temperatures inCaenorhabditis elegans." Genetics 156, no. 3 (2000): 1047–67. http://dx.doi.org/10.1093/genetics/156.3.1047.

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AbstractDauer formation in Caenorhabditis elegans is regulated by several environmental stimuli, including a pheromone and temperature. Dauer formation is moderately induced as the growth temperature increases from 15° to 25°. Here we show that dauer formation is very strongly induced at a temperature of 27° in both wild-type animals and mutants such as unc-64, unc-31, and unc-3, which do not form dauers at 25°. A 27° temperature stimulus is sufficient to induce dauer formation in wild-type animals independent of pheromone. Analysis of previously described dauer mutants at 27° reveals a number of surprising results. Several classes of mutants (dyf, daf-3, tax-4, and tax-2) that are defective in dauer formation at lower temperatures reverse their phenotypes at 27° and form dauers constitutively. Epistasis experiments place unc-64 and unc-31 at a different position in the dauer pathway from unc-3. We also uncover new branches of the dauer pathway at 27° that are not detected at 25°. We show that epistatic gene interactions can show both quantitative and qualitative differences depending on environmental conditions. Finally, we discuss some of the possible ecological implications of dauer induction by high temperatures.

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Vowels, J. J., and J. H. Thomas. "Genetic analysis of chemosensory control of dauer formation in Caenorhabditis elegans." Genetics 130, no. 1 (1992): 105–23. http://dx.doi.org/10.1093/genetics/130.1.105.

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Abstract Dauer larva formation in Caenorhabditis elegans is controlled by chemosensory cells that respond to environmental cues. Genetic interactions among mutations in 23 genes that affect dauer larva formation were investigated. Mutations in seven genes that cause constitutive dauer formation, and mutations in 16 genes that either block dauer formation or result in the formation of abnormal dauers, were analyzed. Double mutants between dauer-constitutive and dauer-defective mutations were constructed and characterized for their capacity to form dauer larvae. Many of the genes could be interpreted to lie in a simple linear epistasis pathway. Three genes, daf-16, daf-18 and daf-20, may affect downstream steps in a branched part of the pathway. Three other genes, daf-2, daf-3 and daf-5, displayed partial or complex epistasis interactions that were difficult to interpret as part of a simple linear pathway. Dauer-defective mutations in nine genes cause structurally defective chemosensory cilia, thereby blocking chemosensation. Mutations in all nine of these genes appear to fall at a single step in the epistasis pathway. Dauer-constitutive mutations in one gene, daf-11, were strongly suppressed for dauer formation by mutations in the nine cilium-structure genes. Mutations in the other six dauer-constitutive genes caused dauer formation despite the absence of functional chemosensory endings. These results suggest that daf-11 is directly involved in chemosensory transduction essential for dauer formation, while the other Daf-c genes play roles downstream of the chemosensory step.

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Lee, James Siho, Pei-Yin Shih, Oren N. Schaedel, Porfirio Quintero-Cadena, Alicia K. Rogers, and Paul W. Sternberg. "FMRFamide-like peptides expand the behavioral repertoire of a densely connected nervous system." Proceedings of the National Academy of Sciences 114, no. 50 (2017): E10726—E10735. http://dx.doi.org/10.1073/pnas.1710374114.

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Animals, including humans, can adapt to environmental stress through phenotypic plasticity. The free-living nematode Caenorhabditis elegans can adapt to harsh environments by undergoing a whole-animal change, involving exiting reproductive development and entering the stress-resistant dauer larval stage. The dauer is a dispersal stage with dauer-specific behaviors for finding and stowing onto carrier animals, but how dauers acquire these behaviors, despite having a physically limited nervous system of 302 neurons, is poorly understood. We compared dauer and reproductive development using whole-animal RNA sequencing at fine time points and at sufficient depth to measure transcriptional changes within single cells. We detected 8,042 genes differentially expressed during dauer and reproductive development and observed striking up-regulation of neuropeptide genes during dauer entry. We knocked down neuropeptide processing using sbt-1 mutants and demonstrate that neuropeptide signaling promotes the decision to enter dauer rather than reproductive development. We also demonstrate that during dauer neuropeptides modulate the dauer-specific nictation behavior (carrier animal-hitchhiking) and are necessary for switching from repulsion to CO2 (a carrier animal cue) in nondauers to CO2 attraction in dauers. We tested individual neuropeptides using CRISPR knockouts and existing strains and demonstrate that the combined effects of flp-10 and flp-17 mimic the effects of sbt-1 on nictation and CO2 attraction. Through meta-analysis, we discovered similar up-regulation of neuropeptides in the dauer-like infective juveniles of diverse parasitic nematodes, suggesting the antiparasitic target potential of SBT-1. Our findings reveal that, under stress, increased neuropeptide signaling in C. elegans enhances their decision-making accuracy and expands their behavioral repertoire.

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Chen, Jianjun, and Edward Caswell-Chen. "Why Caenorhabditis elegans adults sacrifice their bodies to progeny." Nematology 5, no. 4 (2003): 641–45. http://dx.doi.org/10.1163/156854103322683355.

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Abstract We present a novel interpretation regarding the ecology and evolution of matricidal hatching ('bagging') in Caenorhabditis elegans. Subjecting young and mature adult C. elegans to stress induced matricidal hatching. The process of egg retention followed by internal hatching under starvation was reversible, depending on whether adults were returned to food before internal juveniles caused irreversible harm to the adult. We surface sterilised adult C. elegans and then starved them to test the hypothesis that matricidal hatching promotes progeny survival by enhancing to some degree the transition to the dauer stage. When the surface sterilisation stress time was short, the parent C. elegans enclosed many progeny that competed for resources so that apparently only a few progeny obtained sufficient nutrition to support transition to the dauer stage. Longer sterilisation stress and starvation resulted in fewer, larger progeny with a higher proportion reaching the dauer stage, suggesting a direct correlation between the phenomena. In stressful environments, the production of even a single, stress-resistant, long-lived dauer, in lieu of progeny that cannot achieve the dauer, is a fitness advantage. The results are consistent with the hypothesis. We infer that intra-uterine hatch is a part of the C. elegans life cycle, and complements androdioecy and the dauer stage to enhance progeny survival and dispersal under stress. This is a possible explanation of why a seemingly detrimental behaviour, matricidal hatching, has been perpetuated in C. elegans through evolutionary time.

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Ailion, Michael, and James H. Thomas. "Isolation and Characterization of High-Temperature-Induced Dauer Formation Mutants in Caenorhabditis elegans." Genetics 165, no. 1 (2003): 127–44. http://dx.doi.org/10.1093/genetics/165.1.127.

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Abstract Dauer formation in Caenorhabditis elegans is regulated by at least three signaling pathways, including an insulin receptor-signaling pathway. These pathways were defined by mutants that form dauers constitutively (Daf-c) at 25°. Screens for Daf-c mutants at 25° have probably been saturated, but failed to identify all the components involved in regulating dauer formation. Here we screen for Daf-c mutants at 27°, a more strongly dauer-inducing condition. Mutations identified include novel classes of alleles for three known genes and alleles defining at least seven new genes, hid-1–hid-7. Many of the genes appear to act in the insulin branch of the dauer pathway, including pdk-1, akt-1, aex-6, and hid-1. We also molecularly identify hid-1 and show that it encodes a novel highly conserved putative transmembrane protein expressed in neurons.

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van Swinderen, Bruno, Laura B. Metz, Laynie D. Shebester, and C. Michael Crowder. "ACaenorhabditis elegansPheromone Antagonizes Volatile Anesthetic Action Through a Go-Coupled Pathway." Genetics 161, no. 1 (2002): 109–19. http://dx.doi.org/10.1093/genetics/161.1.109.

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AbstractVolatile anesthetics (VAs) disrupt nervous system function by an ill-defined mechanism with no known specific antagonists. During the course of characterizing the response of the nematode C. elegans to VAs, we discovered that a C. elegans pheromone antagonizes the VA halothane. Acute exposure to pheromone rendered wild-type C. elegans resistant to clinical concentrations of halothane, increasing the EC50 from 0.43 ± 0.03 to 0.90 ± 0.02. C. elegans mutants that disrupt the function of sensory neurons required for the action of the previously characterized dauer pheromone blocked pheromone-induced resistance (Pir) to halothane. Pheromone preparations from loss-of-function mutants of daf-22, a gene required for dauer pheromone production, lacked the halothane-resistance activity, suggesting that dauer and Pir pheromone are identical. However, the pathways for pheromone’s effects on dauer formation and VA action were not identical. Not all mutations that alter dauer formation affected the Pir phenotype. Further, mutations in genes not known to be involved in dauer formation completely blocked Pir, including those altering signaling through the G proteins Goα and Gqα. A model in which sensory neurons transduce the pheromone activity through antagonistic Go and Gq pathways, modulating VA action against neurotransmitter release machinery, is proposed.

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Lee, Kyung Eun, Jeong Hoon Cho, and Hyun-Ok Song. "Calumenin, a Ca2+ Binding Protein, Is Required for Dauer Formation in Caenorhabditis elegans." Biology 12, no. 3 (2023): 464. http://dx.doi.org/10.3390/biology12030464.

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Caenorhabditis elegans can adapt and survive in dynamically changing environments by the smart and delicate switching of molecular plasticity. C. elegans dauer diapause is a form of phenotypic and developmental plasticity that induces reversible developmental arrest upon environmental cues. An ER (endoplasmic reticulum)-resident Ca2+ binding protein, calumenin has been reported to function in a variety of malignant diseases in vertebrates and in the process of muscle contraction–relaxation. In C. elegans, CALU-1 is known to function in Ca2+-regulated behaviors (pharyngeal pumping and defecation) and cuticle formation. The cuticles of dauer larvae are morphologically distinct from those of larvae that develop in favorable conditions. The structure of the dauer cuticle is thicker and more highly reinforced than that of other larval stages to protect dauer larvae from various environmental insults. Since the calu-1(tm1783) mutant exhibited abnormal cuticle structures such as highly deformed annuli and alae, we investigated whether CALU-1 is involved in dauer formation or not. Ascaroside pheromone (ascr#2) and crude daumone were used under starvation conditions to analyze the rate of dauer formation in the calu-1(tm1783) mutant. Surprisingly, the dauer ratio of the calu-1(tm1783) mutant was extremely low compared to that of the wild type. In fact, the calu-1(tm1783) mutants were mostly unable to enter diapause. We also found that calu-1 is expressed in body-wall muscle and AIA interneurons at the dauer stage. Taken together, our results suggest that CALU-1 is required for normal entry into diapause in C. elegans.

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Green, James W. M., and Simon C. Harvey. "Development of Caenorhabditis elegans dauer larvae in growing populations." Nematology 14, no. 2 (2012): 165–73. http://dx.doi.org/10.1163/138855411x584115.

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For species that rely on ephemeral resources, genotype fitness will depend on traits that affect both population growth rates and dispersal. Understanding how such traits are related is central to understanding how they may evolve. Natural populations of Caenorhabditis elegans exhibit rapid population growth within resource-rich patches of decaying organic material and subsequent dispersal, primarily as developmentally-arrested dauer larvae, between patches. The properties of growing populations of C. elegans are, however, poorly understood. Here we show that food availability, dauer pheromone (a measure of conspecific population density) and temperature affect dauer larvae development in growing populations as would be predicted from analyses of single cohorts of worms. We also show that as food patch size increases, dauer larvae are formed prior to patch exhaustion and that the number of dauer larvae present increases after the patch is exhausted, i.e., worms that had not completed development as dauer larvae when the food was exhausted continue development in the absence of bacterial food. Crucially, the subsequent reproductive fitness of dauer larvae that complete development after the exhaustion of the bacterial food patch is reduced in comparison with dauer larvae that develop prior to patch exhaustion. These results demonstrate that population level analyses of C. elegans are feasible, support previous studies of the environmental factors affecting dauer larvae development and suggest an adaptive benefit for variation between isolates in the sensitivity of dauer larvae development.

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Harvey, Simon C. "Non-dauer larval dispersal inCaenorhabditis elegans." Journal of Experimental Zoology Part B: Molecular and Developmental Evolution 312B, no. 3 (2009): 224–30. http://dx.doi.org/10.1002/jez.b.21287.

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Dulovic, Alex, Tess Renahan, Waltraud Röseler, Christian Rödelsperger, Ann M. Rose, and Adrian Streit. "Rhabditophanes diutinus a parthenogenetic clade IV nematode with dauer larvae." PLOS Pathogens 16, no. 12 (2020): e1009113. http://dx.doi.org/10.1371/journal.ppat.1009113.

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Comparative studies using non-parasitic model species such as Caenorhabditis elegans, have been very helpful in investigating the basic biology and evolution of parasitic nematodes. However, as phylogenetic distance increases, these comparisons become more difficult, particularly when outside of the nematode clade to which C. elegans belongs (V). One of the reasons C. elegans has nevertheless been used for these comparisons, is that closely related well characterized free-living species that can serve as models for parasites of interest are frequently not available. The Clade IV parasitic nematodes Strongyloides are of great research interest due to their life cycle and other unique biological features, as well as their medical and veterinary importance. Rhabditophanes, a closely related free-living genus, forms part of the Strongyloidoidea nematode superfamily. Rhabditophanes diutinus (= R. sp. KR3021) was included in the recent comparative genomic analysis of the Strongyloididae, providing some insight into the genomic nature of parasitism. However, very little is known about this species, limiting its usefulness as a research model. Here we provide a species description, name the species as R. diutinus and investigate its life cycle and subsequently gene expression in multiple life stages. We identified two previously unreported starvation induced life stages: dauer larvae and arrested J2 (J2A) larvae. The dauer larvae are morphologically similar to and are the same developmental stage as dauers in C. elegans and infective larvae in Strongyloides. As in C. elegans and Strongyloides, dauer formation is inhibited by treatment with dafachronic acid, indicating some genetic control mechanisms are conserved. Similarly, the expression patterns of putative dauer/infective larva control genes resemble each other, in particular between R. diutinus and Strongyloides spp. These findings illustrate and increase the usefulness of R. diutinus as a non-parasitic, easy to work with model species for the Strongyloididae for studying the evolution of parasitism as well as many aspects of the biology of Strongyloides spp, in particular the formation of infective larvae.

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Ewald, Collin Yvès, Jorge Iván Castillo-Quan, and T. Keith Blackwell. "Untangling Longevity, Dauer, and Healthspan in Caenorhabditis elegans Insulin/IGF-1-Signalling." Gerontology 64, no. 1 (2017): 96–104. http://dx.doi.org/10.1159/000480504.

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The groundbreaking discovery that lower levels of insulin/IGF-1 signaling (IIS) can induce lifespan extension was reported 24 years ago in the nematode Caenorhabditis elegans. In this organism, mutations in the insulin/IGF-1 receptor gene daf-2 or other genes in this pathway can double lifespan. Subsequent work has revealed that reduced IIS (rIIS) extends lifespan across diverse species, possibly including humans. In C. elegans, IIS also regulates development into the diapause state known as dauer, a quiescent larval form that enables C. elegans to endure harsh environments through morphological adaptation, improved cellular repair, and slowed metabolism. Considerable progress has been made uncovering mechanisms that are affected by C. elegans rIIS. However, from the beginning it has remained unclear to what extent rIIS extends C. elegans lifespan by mobilizing dauer-associated mechanisms in adults. As we discuss, recent work has shed light on this question by determining that rIIS can extend C. elegans lifespan comparably through downstream processes that are either dauer-related or -independent. Importantly, these two lifespan extension programs can be distinguished genetically. It will now be critical to tease apart these programs, because each may involve different longevity-promoting mechanisms that may be relevant to higher organisms. A recent analysis of organismal “healthspan” has questioned the value of C. elegans rIIS as a paradigm for understanding healthy aging, as opposed to simply extending life. We discuss other work that argues strongly that C. elegans rIIS is indeed an invaluable model and consider the likely possibility that dauer-related processes affect parameters associated with health under rIIS conditions. Together, these studies indicate that C. elegans and analyses of rIIS in this organism will continue to provide unexpected and exciting results, and new paradigms that will be valuable for understanding healthy aging in humans.

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Viney, Mark E., Michael P. Gardner, and Joseph A. Jackson. "Variation in Caenorhabditis elegans dauer larva formation." Development, Growth and Differentiation 45, no. 4 (2003): 389–96. http://dx.doi.org/10.1046/j.1440-169x.2003.00703.x.

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Preusser, Friedrich, Anika Neuschulz, Jan Philipp Junker, Nikolaus Rajewsky, and Stephan Preibisch. "Long-term imaging reveals behavioral plasticity during C. elegans dauer exit." BMC Biology 20, no. 1 (2022): 277. https://doi.org/10.1186/s12915-022-01471-4.

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Background: During their lifetime, animals must adapt their behavior to survive in changing environments. This ability requires the nervous system to undergo adjustments at distinct temporal scales, from short-term dynamic changes in expression of neurotransmitters and receptors to longer-term growth, spatial and connectivity reorganization, while integrating external stimuli. The nematode Caenorhabditis elegans provides a model of nervous system plasticity, in particular its dauer exit decision. Under unfavorable conditions, larvae will enter the non-feeding and non-reproductive stress-resistant dauer stage and adapt their behavior to cope with the harsh new environment, with active reversal under improved conditions leading to resumption of reproductive development. However, how different environmental stimuli regulate the exit decision mechanism and thereby drive the larva's behavioral change is unknown. To fill this gap and provide insights on behavioral changes over extended periods of time, we developed a new open hardware method for long-term imaging (12h) of C. elegans larvae.Results: Our WormObserver platform comprises open hardware and software components for video acquisition, automated processing of large image data (> 80k images/experiment) and data analysis. We identified dauer-specific behavioral motifs and characterized the behavioral trajectory of dauer exit in different environments and genetic backgrounds to identify key decision points and stimuli promoting dauer exit. Combining long-term behavioral imaging with transcriptomics data, we find that bacterial ingestion triggers a change in neuropeptide gene expression to establish post-dauer behavior.Conclusions: Taken together, we show how a developing nervous system can robustly integrate environmental changes activate a developmental switch and adapt the organism's behavior to a new environment. WormObserver is generally applicable to other research questions within and beyond the C. elegans field, having a modular and customizable character and allowing assessment of behavioral plasticity over longer periods.

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Park, D., A. Estevez, and D. L. Riddle. "Antagonistic Smad transcription factors control the dauer/non-dauer switch in C. elegans." Development 137, no. 3 (2010): 477–85. http://dx.doi.org/10.1242/dev.043752.

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McClanahan, Patrick D., Richard J. McCloskey, Melanie Ng Tung Hing, David M. Raizen, and Christopher Fang-Yen. "Dehydrated Caenorhabditis elegans Stocks Are Resistant to Multiple Freeze-Thaw Cycles." G3: Genes|Genomes|Genetics 10, no. 12 (2020): 4505–12. http://dx.doi.org/10.1534/g3.120.401825.

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Ultracold preservation is widely used for storage of genetic stocks of Caenorhabditis elegans. Current cryopreservation protocols are vulnerable to refrigeration failures, which can result in the loss of stock viability due to damage during re-freezing. Here we present a method for preserving worms in a dehydrated and frozen form that retains viability after multiple freeze-thaw cycles. After dehydration in the presence of trehalose or glycerol, C. elegans stocks can be frozen and thawed multiple times while maintaining viability. While both dauer and non-dauer larvae survive desiccation and freezing, the dauer defective mutant daf-16 does not survive desiccation. Our technique is useful for storing stocks in a manner robust to freezer failures, and potentially for shipping strains between laboratories.

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Euling, S., and V. Ambros. "Reversal of cell fate determination in Caenorhabditis elegans vulval development." Development 122, no. 8 (1996): 2507–15. http://dx.doi.org/10.1242/dev.122.8.2507.

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In Caenorhabditis elegans, the fates of the multipotent vulval precursor cells (VPCs) are specified by intercellular signals. The VPCs divide in the third larval stage (L3) of the wild type, producing progeny of determined cell types. In lin-28 mutants, vulva development is similar to wild-type vulva development except that it occurs precociously, in the second larval stage (L2). Consequently, when lin-28 hermaphrodites temporarily arrest development at the end of L2 in the dauer larva stage, they have partially developed vulvae consisting of VPC progeny. During post-dauer development, these otherwise determined VPC progeny become reprogrammed back to the multipotent, signal-sensitive state of VPCs. Our results indicate that VPC fate determination by intercellular signals is reversible by dauer larva developmental arrest and post-dauer development.

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Kandoor, Alekhya, and Janna Fierst. "Dauer fate in a Caenorhabditis elegans Boolean network model." PeerJ 11 (January 23, 2023): e14713. http://dx.doi.org/10.7717/peerj.14713.

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Cellular fates are determined by genes interacting across large, complex biological networks. A critical question is how to identify causal relationships spanning distinct signaling pathways and underlying organismal phenotypes. Here, we address this question by constructing a Boolean model of a well-studied developmental network and analyzing information flows through the system. Depending on environmental signals Caenorhabditis elegans develop normally to sexual maturity or enter a reproductively delayed, developmentally quiescent ‘dauer’ state, progressing to maturity when the environment changes. The developmental network that starts with environmental signal and ends in the dauer/no dauer fate involves genes across 4 signaling pathways including cyclic GMP, Insulin/IGF-1, TGF-β and steroid hormone synthesis. We identified three stable motifs leading to normal development, each composed of genes interacting across the Insulin/IGF-1, TGF-β and steroid hormone synthesis pathways. Three genes known to influence dauer fate, daf-2, daf-7 and hsf-1, acted as driver nodes in the system. Using causal logic analysis, we identified a five gene cyclic subgraph integrating the information flow from environmental signal to dauer fate. Perturbation analysis showed that a multifactorial insulin profile determined the stable motifs the system entered and interacted with daf-12 as the switchpoint driving the dauer/no dauer fate. Our results show that complex organismal systems can be distilled into abstract representations that permit full characterization of the causal relationships driving developmental fates. Analyzing organismal systems from this perspective of logic and function has important implications for studies examining the evolution and conservation of signaling pathways.

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Larsen, P. L., P. S. Albert, and D. L. Riddle. "Genes that regulate both development and longevity in Caenorhabditis elegans." Genetics 139, no. 4 (1995): 1567–83. http://dx.doi.org/10.1093/genetics/139.4.1567.

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Abstract The nematode Caenorhabditis elegans responds to conditions of overcrowding and limited food by arresting development as a dauer larva. Genetic analysis of mutations that alter dauer larva formation (daf mutations) is presented along with an updated genetic pathway for dauer vs. nondauer development. Mutations in the daf-2 and daf-23 genes double adult life span, whereas mutations in four other dauer-constitutive genes positioned in a separate branch of this pathway (daf-1, daf-4, daf-7 and daf-8) do not. The increased life spans are suppressed completely by a daf-16 mutation and partially in a daf-2; daf-18 double mutant. A genetic pathway for determination of adult life span is presented based on the same strains and growth conditions used to characterize Daf phenotypes. Both dauer larva formation and adult life span are affected in daf-2; daf-12 double mutants in an allele-specific manner. Mutations in daf-12 do not extend adult life span, but certain combinations of daf-2 and daf-12 mutant alleles nearly quadruple it. This synergistic effect, which does not equivalently extend the fertile period, is the largest genetic extension of life span yet observed in a metazoan.

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Gelmedin, Verena, Thomas Brodigan, Xin Gao, Michael Krause, Zhu Wang, and John M. Hawdon. "Transgenic C. elegans Dauer Larvae Expressing Hookworm Phospho Null DAF-16/FoxO Exit Dauer." PLoS ONE 6, no. 10 (2011): e25996. http://dx.doi.org/10.1371/journal.pone.0025996.

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Zwaal, Richard R., Jane E. Mendel, Paul W. Sternberg, and Ronald H. A. Plasterk. "Two Neuronal G Proteins are Involved in Chemosensation of the Caenorhabditis elegans Dauer-Inducing Pheromone." Genetics 145, no. 3 (1997): 715–27. http://dx.doi.org/10.1093/genetics/145.3.715.

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Caenorhabditis elegans uses chemosensation to determine its course of development. Young larvae can arrest as dauer larvae in response to increasing population density, which they measure by a nematode-excreted pheromone, and decreasing food supply. Dauer larvae can resume development in response to a decrease in pheromone and increase in food concentration. We show here that two novel G protein alpha subunits (GPA-2 and GPA-3) show promoter activity in subsets of chemosensory neurons and are involved in the decision to form dauer larvae primarily through the response to dauer pheromone. Dominant activating mutations in these G proteins result in constitutive, pheromone-independent dauer formation, whereas inactivation results in reduced sensitivity to pheromone, and, under certain conditions, an alteration in the response to food. Interactions between gpa-2, gpa-3 and other genes controlling dauer formation suggest that these G proteins may act in parallel to regulate the neuronal decision making that precedes dauer formation.

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Joo, Hyoe-Jin, Yong-Hyeon Yim, Pan-Young Jeong, et al. "Caenorhabditis elegans utilizes dauer pheromone biosynthesis to dispose of toxic peroxisomal fatty acids for cellular homoeostasis." Biochemical Journal 422, no. 1 (2009): 61–71. http://dx.doi.org/10.1042/bj20090513.

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Caenorhabditis elegans excretes a dauer pheromone or daumone composed of ascarylose and a fatty acid side chain, the perception of which enables worms to enter the dauer state for long-term survival in an adverse environment. During the course of elucidation of the daumone biosynthetic pathway in which DHS-28 and DAF-22 are involved in peroxisomal β-oxidation of VLCFAs (very long-chain fatty acids), we sought to investigate the physiological consequences of a deficiency in daumone biosynthesis in C. elegans. Our results revealed that two mutants, dhs-28(tm2581) and daf-22(ok693), lacked daumones and thus were dauer defective; this coincided with massive accumulation of fatty acyl-CoAs (up to 100-fold) inside worm bodies compared with levels in wild-type N2 worms. Furthermore, the deficiency in daumone biosynthesis and the massive accumulation of fatty acids and their acyl-CoAs caused severe developmental defects with reduced life spans (up to 30%), suggesting that daumone biosynthesis is be an essential part of C. elegans homoeostasis, affecting survival and maintenance of optimal physiological conditions by metabolizing some of the toxic non-permissible peroxisomal VLCFAs from the worm body in the form of readily excretable daumones.

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Daniels, Susan A., Michael Ailion, James H. Thomas та Piali Sengupta. "egl-4 Acts Through a Transforming Growth Factor-β/SMAD Pathway in Caenorhabditis elegans to Regulate Multiple Neuronal Circuits in Response to Sensory Cues". Genetics 156, № 1 (2000): 123–41. http://dx.doi.org/10.1093/genetics/156.1.123.

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Abstract Sensory cues regulate several aspects of behavior and development in Caenorhabditis elegans, including entry into and exit from an alternative developmental stage called the dauer larva. Three parallel pathways, including a TGF-β-like pathway, regulate dauer formation. The mechanisms by which the activities of these pathways are regulated by sensory signals are largely unknown. The gene egl-4 was initially identified based on its egg-laying defects. We show here that egl-4 has many pleiotropies, including defects in chemosensory behavior, body size, synaptic transmission, and dauer formation. Our results are consistent with a role for egl-4 in relaying sensory cues to multiple behavioral and developmental circuits in C. elegans. By epistasis analysis, we also place egl-4 in the TGF-β-like branch and show that a SMAD gene functions downstream of egl-4 in multiple egl-4-regulated pathways, including chemosensation.

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Wong, Christopher, and Richard Roy. "AMPK Regulates Developmental Plasticity through an Endogenous Small RNA Pathway in Caenorhabditis elegans." International Journal of Molecular Sciences 21, no. 6 (2020): 2238. http://dx.doi.org/10.3390/ijms21062238.

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Caenorhabditis elegans larvae can undergo developmental arrest upon entry into the dauer stage in response to suboptimal growth conditions. Dauer larvae can exit this stage in replete conditions with no reproductive consequence. During this diapause stage, the metabolic regulator AMP-activated protein kinase (AMPK) ensures that the germ line becomes quiescent to maintain germ cell integrity. Animals that lack all AMPK signalling undergo germline hyperplasia upon entering dauer, while those that recover from this stage become sterile. Neuronal AMPK expression in otherwise AMPK-deficient animals is sufficient for germline quiescence and germ cell integrity and its effects are likely mediated through an endogenous small RNA pathway. Upon impairing small RNA biosynthesis, the post-dauer fertility is restored in AMPK mutants. These data suggest that AMPK may function in neurons to relay a message through small RNAs to the germ cells to alter their quiescence in the dauer stage, thus challenging the permeability of the Weismann barrier.

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Witting, Michael, Ulrike Schmidt, and Hans-Joachim Knölker. "UHPLC-IM-Q-ToFMS analysis of maradolipids, found exclusively in Caenorhabditis elegans dauer larvae." Analytical and Bioanalytical Chemistry 413, no. 8 (2021): 2091–102. http://dx.doi.org/10.1007/s00216-021-03172-3.

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AbstractLipid identification is one of the current bottlenecks in lipidomics and lipid profiling, especially for novel lipid classes, and requires multidimensional data for correct annotation. We used the combination of chromatographic and ion mobility separation together with data-independent acquisition (DIA) of tandem mass spectrometric data for the analysis of lipids in the biomedical model organism Caenorhabditis elegans. C. elegans reacts to harsh environmental conditions by interrupting its normal life cycle and entering an alternative developmental stage called dauer stage. Dauer larvae show distinct changes in metabolism and morphology to survive unfavorable environmental conditions and are able to survive for a long time without feeding. Only at this developmental stage, dauer larvae produce a specific class of glycolipids called maradolipids. We performed an analysis of maradolipids using ultrahigh performance liquid chromatography-ion mobility spectrometry-quadrupole-time of flight-mass spectrometry (UHPLC-IM-Q-ToFMS) using drift tube ion mobility to showcase how the integration of retention times, collisional cross sections, and DIA fragmentation data can be used for lipid identification. The obtained results show that combination of UHPLC and IM separation together with DIA represents a valuable tool for initial lipid identification. Using this analytical tool, a total of 45 marado- and lysomaradolipids have been putatively identified and 10 confirmed by authentic standards directly from C. elegans dauer larvae lipid extracts without the further need for further purification of glycolipids. Furthermore, we putatively identified two isomers of a lysomaradolipid not known so far. Graphical abstract

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McClanahan, Patrick D., Luca Golinelli, Tuan Anh Le, and Liesbet Temmerman. "Automated scoring of nematode nictation on a textured background." PLOS ONE 18, no. 8 (2023): e0289326. http://dx.doi.org/10.1371/journal.pone.0289326.

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Entomopathogenic nematodes, including Steinernema spp., play an increasingly important role as biological alternatives to chemical pesticides. The infective juveniles of these worms use nictation–a behavior in which animals stand on their tails–as a host-seeking strategy. The developmentally-equivalent dauer larvae of the free-living nematode Caenorhabditis elegans also nictate, but as a means of phoresy or "hitching a ride" to a new food source. Advanced genetic and experimental tools have been developed for C. elegans, but time-consuming manual scoring of nictation slows efforts to understand this behavior, and the textured substrates required for nictation can frustrate traditional machine vision segmentation algorithms. Here we present a Mask R-CNN-based tracker capable of segmenting C. elegans dauers and S. carpocapsae infective juveniles on a textured background suitable for nictation, and a machine learning pipeline that scores nictation behavior. We use our system to show that the nictation propensity of C. elegans from high-density liquid cultures largely mirrors their development into dauers, and to quantify nictation in S. carpocapsae infective juveniles in the presence of a potential host. This system is an improvement upon existing intensity-based tracking algorithms and human scoring which can facilitate large-scale studies of nictation and potentially other nematode behaviors.

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Wirick, Matthew J., Allison R. Cale, Isaac T. Smith, et al. "daf-16/FOXO blocks adult cell fate in Caenorhabditis elegans dauer larvae via lin-41/TRIM71." PLOS Genetics 17, no. 11 (2021): e1009881. http://dx.doi.org/10.1371/journal.pgen.1009881.

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Many tissue-specific stem cells maintain the ability to produce multiple cell types during long periods of non-division, or quiescence. FOXO transcription factors promote quiescence and stem cell maintenance, but the mechanisms by which FOXO proteins promote multipotency during quiescence are still emerging. The single FOXO ortholog in C. elegans, daf-16, promotes entry into a quiescent and stress-resistant larval stage called dauer in response to adverse environmental cues. During dauer, stem and progenitor cells maintain or re-establish multipotency to allow normal development to resume after dauer. We find that during dauer, daf-16/FOXO prevents epidermal stem cells (seam cells) from prematurely adopting differentiated, adult characteristics. In particular, dauer larvae that lack daf-16 misexpress collagens that are normally adult-enriched. Using col-19p::gfp as an adult cell fate marker, we find that all major daf-16 isoforms contribute to opposing col-19p::gfp expression during dauer. By contrast, daf-16(0) larvae that undergo non-dauer development do not misexpress col-19p::gfp. Adult cell fate and the timing of col-19p::gfp expression are regulated by the heterochronic gene network, including lin-41 and lin-29. lin-41 encodes an RNA-binding protein orthologous to LIN41/TRIM71 in mammals, and lin-29 encodes a conserved zinc finger transcription factor. In non-dauer development, lin-41 opposes adult cell fate by inhibiting the translation of lin-29, which directly activates col-19 transcription and promotes adult cell fate. We find that during dauer, lin-41 blocks col-19p::gfp expression, but surprisingly, lin-29 is not required in this context. Additionally, daf-16 promotes the expression of lin-41 in dauer larvae. The col-19p::gfp misexpression phenotype observed in dauer larvae with reduced daf-16 requires the downregulation of lin-41, but does not require lin-29. Taken together, this work demonstrates a novel role for daf-16/FOXO as a heterochronic gene that promotes expression of lin-41/TRIM71 to contribute to multipotent cell fate in a quiescent stem cell model.

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Malone, E. A., and J. H. Thomas. "A screen for nonconditional dauer-constitutive mutations in Caenorhabditis elegans." Genetics 136, no. 3 (1994): 879–86. http://dx.doi.org/10.1093/genetics/136.3.879.

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Abstract In Caenorhabditis elegans, formation of the developmentally arrested dauer larva is induced by high levels of a constitutively secreted pheromone. Synergy between two groups of incompletely penetrant dauer-constitutive (Daf-c) mutations has recently led to a proposal that these two groups of genes are partially redundant and function in two parallel pathways that regulate dauer formation. A possible weakness in this reasoning is that the mutations used to identify the synergy were specifically obtained as incompletely penetrant mutations. Here we use screens to identify new Daf-c alleles without any requirement for partial penetrance. Nevertheless, 22 of the 25 new mutations are incompletely penetrant mutations in 6 previously identified genes. Among these are mutations in daf-8 and daf-19, genes for which only one mutation had been previously identified. Also included in this group are three daf-1 alleles that do not exhibit the maternal rescue characteristic of other daf-1 alleles. Two of the 25 new mutations are fully penetrant and are alleles of daf-2, the one gene in which a fully penetrant mutation had been found earlier. Finally, one of the 25 new mutations is semidominant, temperature-sensitive, and identifies a new gene, daf-28. The results demonstrate that an incompletely penetrant Daf-c phenotype is characteristic of mutations in most Daf-c genes other than daf-2. This finding strengthens the hypothesis that a branched genetic pathway controls dauer formation.

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ONODERA, Akira, Sumino YANASE, Takamasa ISHII, et al. "Post-dauer Life Span of Caenorhabditis Elegans Dauer Larvae Can be Modified by X-irradiation." Journal of Radiation Research 51, no. 1 (2010): 67–71. http://dx.doi.org/10.1269/jrr.09093.

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Tissenbaum, Heidi A., and Gary Ruvkun. "An Insulin-like Signaling Pathway Affects Both Longevity and Reproduction in Caenorhabditis elegans." Genetics 148, no. 2 (1998): 703–17. http://dx.doi.org/10.1093/genetics/148.2.703.

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Abstract Mutations in daf-2 and age-1 cause a dramatic increase in longevity as well as developmental arrest at the dauer diapause stage in Caenorhabditis elegans. daf-2 and age-1 encode components of an insulin-like signaling pathway. Both daf-2 and age-1 act at a similar point in the genetic epistasis pathway for dauer arrest and longevity and regulate the activity of the daf-16 gene. Mutations in daf-16 cause a dauer-defective phenotype and are epistatic to the diapause arrest and life span extension phenotypes of daf-2 and age-1 mutants. Here we show that mutations in this pathway also affect fertility and embryonic development. Weak daf-2 alleles, and maternally rescued age-1 alleles that cause life span extension but do not arrest at the dauer stage, also reduce fertility and viability. We find that age-1(hx546) has reduced both maternal and zygotic age-1 activity. daf-16 mutations suppress all of the daf-2 and age-1 phenotypes, including dauer arrest, life span extension, reduced fertility, and viability defects. These data show that insulin signaling, mediated by DAF-2 through the AGE-1 phosphatidylinositol-3-OH kinase, regulates reproduction and embryonic development, as well as dauer diapause and life span, and that DAF-16 transduces these signals. The regulation of fertility, life span, and metabolism by an insulin-like signaling pathway is similar to the endocrine regulation of metabolism and fertility by mammalian insulin signaling.

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COLONIUS, KERSTIN. "THE DAUER MUTATION OF THE CAENORHABDITIS ELEGANS, SIMULATED WITH THE PENNA AND THE STAUFFER MODELS." International Journal of Modern Physics C 15, no. 07 (2004): 939–45. http://dx.doi.org/10.1142/s0129183104006364.

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Two aging models were analyzed on whether they can confirm the dauer mutation of the nematode helps to preserve the species. As a result the Penna model shows that populations with dauer larvae survive bad environmental conditions, whereas populations without it die out. In the Stauffer model, the advantage of the dauer mutation for the survival is only given under certain conditions.

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Lee, Jeeyong, Kwang-Youl Kim, Jihyun Lee, and Young-Ki Paik. "Regulation of Dauer Formation byO-GlcNAcylation in Caenorhabditis elegans." Journal of Biological Chemistry 285, no. 5 (2009): 2930–39. http://dx.doi.org/10.1074/jbc.m109.022665.

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Wang, J. "Global analysis of dauer gene expression in Caenorhabditis elegans." Development 130, no. 8 (2003): 1621–34. http://dx.doi.org/10.1242/dev.00363.

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Albert, Patrice S., and Donald L. Riddle. "Mutants of Caenorhabditis elegans that form dauer-like larvae." Developmental Biology 126, no. 2 (1988): 270–93. http://dx.doi.org/10.1016/0012-1606(88)90138-8.

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Viney, M. E., and N. R. Franks. "Is dauer pheromone of Caenorhabditis elegans really a pheromone?" Naturwissenschaften 91, no. 3 (2004): 123–24. http://dx.doi.org/10.1007/s00114-004-0503-2.

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Malone, Elizabeth A., Takao Inoue, and James H. Thomas. "Genetic Analysis of the Roles of daf28 and age-1 in Regulating Caenorhabditis elegans Dauer Formation." Genetics 143, no. 3 (1996): 1193–205. http://dx.doi.org/10.1093/genetics/143.3.1193.

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Abstract Based on environmental cues, the nervous system of Caenorhabditis ekgans regulates formation of the dauer larva, an alternative larval form specialized for long-term survival under harsh conditions. Mutations that cause constitutive or defective dauer formation (Daf-c or Daf-d) have been identified and the genes ordered in a branched pathway. Most Daf-c mutations also affect recovery from the dauer stage. The semidominant mutation daf-28(sa191) is Daf-c but has no apparent effect on dauer recovery. We use this unique aspect of daf28(sal91) to characterize the effects of several Daf-d and synthetic Daf-c mutations on dauer recovery. We present double mutant analysis that indicates that daf-28(saI91) acts at a novel point downstream in the genetic pathway for dauer formation. We also show that daf-28(sa191) causes a modest increase (12-13%) in life span. The phenotypes and genetic interactions of daf-28(sa191) are most similar to those of daf-2 and daf-23 mutations, which also cause a dramatic increase in life span. We present mapping and complementation data that suggest that daf-23 is the same gene as age-I, identified previously by mutations that extend life span. We find that age-l alleles are also Daf-c at 27°.

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Gottlieb, S., and G. Ruvkun. "daf-2, daf-16 and daf-23: genetically interacting genes controlling Dauer formation in Caenorhabditis elegans." Genetics 137, no. 1 (1994): 107–20. http://dx.doi.org/10.1093/genetics/137.1.107.

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Abstract Under conditions of high population density and low food, Caenorhabditis elegans forms an alternative third larval stage, called the dauer stage, which is resistant to desiccation and harsh environments. Genetic analysis of some dauer constitutive (Daf-c) and dauer defective (Daf-d) mutants has revealed a complex pathway that is likely to function in particular neurons and/or responding tissues. Here we analyze the genetic interactions between three genes which comprise a branch of the dauer formation pathway that acts in parallel to or downstream of the other branches of the pathway, the Daf-c genes daf-2 and daf-23 and the Daf-d gene daf-16. Unlike mutations in other Daf-c genes, mutations in both daf-2 and daf-23 cause non-conditional arrest at the dauer stage. Our epistasis analysis suggests that daf-2 and daf-23 are functioning at a similar point in the dauer pathway. First, mutations in daf-2 and daf-23 are epistatic to mutations in the same set of Daf-d genes. Second, daf-2 and daf-23 mutants are suppressed by mutations in daf-16. Mutations in daf-16 do not suppress any of the other Daf-c mutants as efficiently as they suppress daf-2 and daf-23 mutants. Third, double mutants between either daf-2 or daf-23 and several other daf-d mutants exhibit an unusual interaction. Based on these results, we present a model for the function of daf-2, daf-23 and daf-16 in dauer formation.

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Mayer, Melanie G., and Ralf J. Sommer. "Natural variation in Pristionchus pacificus dauer formation reveals cross-preference rather than self-preference of nematode dauer pheromones." Proceedings of the Royal Society B: Biological Sciences 278, no. 1719 (2011): 2784–90. http://dx.doi.org/10.1098/rspb.2010.2760.

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Many free-living nematodes, including the laboratory model organisms Caenorhabditis elegans and Pristionchus pacificus , have a choice between direct and indirect development, representing an important case of phenotypic plasticity. Under harsh environmental conditions, these nematodes form dauer larvae, which arrest development, show high resistance to environmental stress and constitute a dispersal stage. Pristionchus pacificus occurs in a strong association with scarab beetles in the wild and remains in the dauer stage on the living beetle. Here, we explored the circumstances under which P. pacificus enters and exits the dauer stage by using a natural variation approach. The analysis of survival, recovery and fitness after dauer exit of eight P. pacificus strains revealed that dauer larvae can survive for up to 1 year under experimental conditions. In a second experiment, we isolated dauer pheromones from 16 P. pacificus strains, and tested for natural variation in pheromone production and sensitivity in cross-reactivity assays. Surprisingly, 13 of the 16 strains produce a pheromone that induces the highest dauer formation in individuals of other genotypes. These results argue against a simple adaptation model for natural variation in dauer formation and suggest that strains may have evolved to induce dauer formation precociously in other strains in order to reduce the fitness of these strains. We therefore discuss intraspecific competition among genotypes as a previously unconsidered aspect of dauer formation.

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Balson, Jordan, Jeffrey R. Boudreau, Ian D. Chin-Sang, Yuxiang Wang, and Daniel D. Lefebvre. "Tolerance to a Diet of Toxic Microcystis aeruginosa in Caenorhabditis elegans." Toxins 17, no. 3 (2025): 109. https://doi.org/10.3390/toxins17030109.

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Reported incidences of cyanobacterial harmful algal blooms (CHABs) are increasing across the world due to climate change and nutrient loading, dominating freshwater ecosystems and producing dangerous cyanotoxins that cause ecological damage. Microcystis aeruginosa is one of the most common species of cyanobacteria; it produces hepatotoxic and neurotoxic microcystin-LR. The ecological and human impact of algal blooms is immense, and traditional CHAB remediation methods are not always adequate in eutrophic regions such as Lake Erie in North America. As a result, a proactive, targeted approach is needed to bioremediate cyanobacteria in their pre-colonial stages. Nematodes, such as the model organism Caenorhabditis elegans, are potential candidates for bioremediating cyanobacteria such as M. aeruginosa. C. elegans have metabolic pathways that could detoxify microcystin-LR and enable tolerance to cyanobacteria in nature. We analyzed C. elegans health and fat accumulation on a diet of toxic M. aeruginosa and found that C. elegans can ingest, digest, metabolize, and survive off of this diet. The mean lifespans of the worm populations were only slightly different at 20.68 ± 0.35 (mean ± S.E.M) and 17.89 ± 0.40 when fed E. coli and toxic M. aeruginosa, respectively. In addition, a diet of toxic M. aeruginosa compared to E. coli did not have any significant impact on C. elegans pharyngeal pumping (304.2 ± 9.3 versus 330.0 ± 10.4 pumps/min), dauer response (86.3 ± 1.0 versus 83.65 ± 1.0% in dauer), mobility (209.25 ± 7.0 versus 210.15 ± 4.4 thrashes/min), or SKN-1 expression based on SKN1::GFP fluorescence measurements. Overall, a diet of toxic M. aeruginosa was able to sustain C. elegans development, and C. elegans was tolerant of it. These results suggest that C. elegans and similar nematodes could be viable candidates for cyanobacterial bioremediation.

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Antebi, A., J. G. Culotti, and E. M. Hedgecock. "daf-12 regulates developmental age and the dauer alternative in Caenorhabditis elegans." Development 125, no. 7 (1998): 1191–205. http://dx.doi.org/10.1242/dev.125.7.1191.

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From egg through adult, C. elegans has six life stages including an option for dauer formation and diapause at larval stage L3 in adverse environments. Somatic cells throughout the organism make consistent choices and advance in unison, suggesting a mechanism of coordinate regulation at these stage transitions. Earlier studies showed that daf-12, which encodes a nuclear receptor (W. Yeh, 1991, Doctoral Thesis. University of Missouri-Columbia), regulates dauer formation; epistasis experiments placed daf-12 near the end of the dauer signaling pathway. Here we describe novel daf-12 alleles that reveal a general role in advancing L3 stage programs. In these mutants, somatic cells repeat L2-specific cellular programs of division and migration at the L3 stage; epistasis experiments place daf-12 between lin-14 and lin-28 within the heterochronic pathway. We propose daf-12 and other heterochronic genes provide cellular memories of chronological stage for selecting stage-appropriate developmental programs. Endocrine factors could coordinate these stage transitions and specify developmental alternatives.

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Thomas, J. H., D. A. Birnby, and J. J. Vowels. "Evidence for parallel processing of sensory information controlling dauer formation in Caenorhabditis elegans." Genetics 134, no. 4 (1993): 1105–17. http://dx.doi.org/10.1093/genetics/134.4.1105.

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Abstract Dauer formation in Caenorhabditis elegans is induced by chemosensation of high levels of a constitutively secreted pheromone. Seven genes defined by mutations that confer a dauer-formation constitutive phenotype (Daf-c) can be congruently divided into two groups by any of three criteria. Group 1 genes (daf-11 and daf-21) are (1) strongly synergistic with group 2 genes for their Daf-c phenotype, (2) incompletely suppressed by dauer-formation defective (Daf-d) mutations in the genes daf-3 and daf-5 and (3) strongly suppressed by Daf-d mutations in nine genes that affect the structure of chemosensory endings. Group 2 genes (daf-1, daf-4, daf-7, daf-8 and daf-14) are (1) strongly synergistic with group 1 genes for their Daf-c phenotype, (2) fully suppressed by Daf-d mutations in daf-3 and daf-5 and (3) not suppressed by Daf-d mutations in the nine genes that affect chemosensory ending structure. Mutations in each group of genes also cause distinct additional behavioral defects. We propose that these two groups of Daf-c genes act in parallel pathways that process sensory information. The two pathways are partially redundant with each other and normally act in concert to control dauer formation.

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Lee, Jeeyong, Kwang-Youl Kim, and Young-Ki Paik. "Alteration in cellular acetylcholine influences dauer formation in Caenorhabditis elegans." BMB Reports 47, no. 2 (2014): 80–85. http://dx.doi.org/10.5483/bmbrep.2014.47.2.100.

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Kim, Kyoohyun, Vamshidhar R. Gade, Teymuras V. Kurzchalia, and Jochen Guck. "Quantitative imaging of Caenorhabditis elegans dauer larvae during cryptobiotic transition." Biophysical Journal 121, no. 7 (2022): 1219–29. http://dx.doi.org/10.1016/j.bpj.2022.02.031.

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Butcher, Rebecca A., Masaki Fujita, Frank C. Schroeder, and Jon Clardy. "Small-molecule pheromones that control dauer development in Caenorhabditis elegans." Nature Chemical Biology 3, no. 7 (2007): 420–22. http://dx.doi.org/10.1038/nchembio.2007.3.

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Fielenbach, N., and A. Antebi. "C. elegans dauer formation and the molecular basis of plasticity." Genes & Development 22, no. 16 (2008): 2149–65. http://dx.doi.org/10.1101/gad.1701508.

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Inoue, Takao, та James H. Thomas. "Targets of TGF-β Signaling in Caenorhabditis elegans Dauer Formation". Developmental Biology 217, № 1 (2000): 192–204. http://dx.doi.org/10.1006/dbio.1999.9545.

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Penkov, Sider, Fanny Mende, Vyacheslav Zagoriy, et al. "Maradolipids: Diacyltrehalose Glycolipids Specific to Dauer Larva in Caenorhabditis elegans." Angewandte Chemie International Edition 49, no. 49 (2010): 9430–35. http://dx.doi.org/10.1002/anie.201004466.

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Penkov, Sider, Fanny Mende, Vyacheslav Zagoriy, et al. "Maradolipids: Diacyltrehalose Glycolipids Specific to Dauer Larva in Caenorhabditis elegans." Angewandte Chemie 122, no. 49 (2010): 9620–25. http://dx.doi.org/10.1002/ange.201004466.

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Banfield, K. L., T. A. Gomez, W. Lee, S. Clarke, and P. L. Larsen. "Protein-Repair and Hormone-Signaling Pathways Specify Dauer and Adult Longevity and Dauer Development in Caenorhabditis elegans." Journals of Gerontology Series A: Biological Sciences and Medical Sciences 63, no. 8 (2008): 798–808. http://dx.doi.org/10.1093/gerona/63.8.798.

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Thatcher, J. D., C. Haun, and P. G. Okkema. "The DAF-3 Smad binds DNA and represses gene expression in the Caenorhabditis elegans pharynx." Development 126, no. 1 (1999): 97–107. http://dx.doi.org/10.1242/dev.126.1.97.

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Gene expression in the pharyngeal muscles of Caenorhabditis elegans is controlled in part by organ-specific signals, which in the myo-2 gene target a short DNA sequence termed the C subelement. To identify genes contributing to these signals, we performed a yeast one-hybrid screen for cDNAs encoding factors that bind the C subelement. One clone recovered was from daf-3, which encodes a Smad most closely related to vertebrate Smad4. We demonstrated that DAF-3 binds C subelement DNA directly and specifically using gel mobility shift and DNase1 protection assays. Mutation of any base in the sequence GTCTG interfered with binding in the gel mobility shift assay, demonstrating that this pentanucleotide is a core recognition sequence for DAF-3 binding. daf-3 is known to promote formation of dauer larvae and this activity is negatively regulated by TGFbeta-like signaling. To determine how daf-3 affects C subelement enhancer activity in vivo, we examined expression a gfp reporter controlled by a concatenated C subelement oligonucleotide in daf-3 mutants and other mutants affecting the TGFbeta-like signaling pathway controlling dauer formation. Our results demonstrate that wild-type daf-3 can repress C subelement enhancer activity during larval development and, like its dauer-promoting activity, daf-3's repressor activity is negatively regulated by TGFbeta-like signaling. We have examined expression of this gfp reporter in dauer larvae and have observed no daf-3-dependent repression of C activity. These results suggest daf-3 directly regulates pharyngeal gene expression during non-dauer development.

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Keane, John, and Leon Avery. "Mechanosensory Inputs Influence Caenorhabditis elegans Pharyngeal Activity via Ivermectin Sensitivity Genes." Genetics 164, no. 1 (2003): 153–62. http://dx.doi.org/10.1093/genetics/164.1.153.

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Abstract Mechanical stimulation induces opposite behavioral responses in the adult and dauer pharynx. Tail tap of adults inhibits pharyngeal pumping via a pathway involving the innexin gene unc-7 and components of the glutamatergic pathway encoded by the genes avr-14 and avr-15. Tail tap of dauers stimulates pumping through a mechanism involving Gαo and Gαq. The nematocidal drug ivermectin is believed to kill worms by opening a glutamate-gated chloride channel (AVR-15) on pharyngeal muscle, causing complete pumping inhibition. However, ivermectin can also inhibit pumping in the absence of this channel. We propose that one of the ways ivermectin could prevent pumping, in the absence of the AVR-15 ivermectin-binding channel on pharynx muscle, is to target AVR-14 and AVR-15, which are expressed in the inhibitory pathway linking mechanosensation and pumping activity.

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