scholarly journals Trimethylamine modulates dauer formation, neurodegeneration, and lifespan through tyra‐3/daf‐11 signaling in Caenorhabditis elegans

Aging Cell ◽  
2021 ◽  
Author(s):  
Amit Khanna ◽  
Durai Sellegounder ◽  
Jitendra Kumar ◽  
Manish Chamoli ◽  
Miguel Vargas ◽  
...  
Keyword(s):  
Caenorhabditis Elegans ◽  
Dauer Formation

Dafadine inhibits DAF-9 to promote dauer formation and longevity of Caenorhabditis elegans

2011 ◽  
Vol 7 (12) ◽  
pp. 891-893 ◽  
Author(s):  
Genna M Luciani ◽  
Lilia Magomedova ◽  
Rachel Puckrin ◽  
Malene L Urbanus ◽  
Iain M Wallace ◽  
...  
Keyword(s):  
Caenorhabditis Elegans ◽  
Dauer Formation

scholarly journals A functional study of all 40 Caenorhabditis elegans insulin-like peptides

2018 ◽  
Vol 293 (43) ◽  
pp. 16912-16922 ◽  
Author(s):  
Shanqing Zheng ◽  
Hilton Chiu ◽  
Jeffrey Boudreau ◽  
Tony Papanicolaou ◽  
William Bendena ◽  
...  
Keyword(s):  
Caenorhabditis Elegans ◽  
Life Span ◽  
Peptide Ligands ◽  
Peptide Sequence ◽  
Functional Study ◽  
C Elegans ◽  
Multiple Phenotypes ◽  
Dauer Formation ◽  
Pleiotropic Function

The human genome encodes 10 insulin-like genes, whereas the Caenorhabditis elegans genome remarkably encodes 40 insulin-like genes. Knockout strategies to determine the roles of all the insulin/insulin-like peptide ligands (INS) in C. elegans has been challenging due to functional redundancy. Here, we individually overexpressed each of the 40 ins genes pan-neuronally, and monitored multiple phenotypes including: L1 arrest life span, neuroblast divisions under L1 arrest, dauer formation, and fat accumulation, as readouts to characterize the functions of each INS in vivo. Of the 40 INS peptides, we found functions for 35 INS peptides and functionally categorized each as agonists, antagonists, or of pleiotropic function. In particular, we found that 9 of 16 agonistic INS peptides shortened L1 arrest life span and promoted neuroblast divisions during L1 arrest. Our study revealed that a subset of β-class INS peptides that contain a distinct F peptide sequence are agonists. Our work is the first to categorize the structures of INS peptides and relate these structures to the functions of all 40 INS peptides in vivo. Our findings will promote the study of insulin function on development, metabolism, and aging-related diseases.

Targets of DAF-16 involved in Caenorhabditis elegans adult longevity and dauer formation

2006 ◽  
Vol 41 (10) ◽  
pp. 922-927 ◽  
Author(s):  
Victor L. Jensen ◽  
Marco Gallo ◽  
Donald L. Riddle
Keyword(s):  
Caenorhabditis Elegans ◽  
Adult Longevity ◽  
Dauer Formation

scholarly journals Genetic analysis of chemosensory control of dauer formation in Caenorhabditis elegans.

Genetics ◽  
1992 ◽  
Vol 130 (1) ◽  
pp. 105-123 ◽  
Author(s):  
J J Vowels ◽  
J H Thomas
Keyword(s):  
Caenorhabditis Elegans ◽  
Genetic Analysis ◽  
Single Step ◽  
Genetic Interactions ◽  
The Other ◽  
Environmental Cues ◽  
Dauer Larva ◽  
Chemosensory Transduction ◽  
Dauer Formation ◽  
Dauer Larvae

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.

scholarly journals Feeding state-dependent regulation of developmental plasticity via CaMKI and neuroendocrine signaling

eLife ◽  
2015 ◽  
Vol 4 ◽  
Author(s):  
Scott J Neal ◽  
Asuka Takeishi ◽  
Michael P O'Donnell ◽  
JiSoo Park ◽  
Myeongjin Hong ◽  
...  
Keyword(s):  
Caenorhabditis Elegans ◽  
Subcellular Localization ◽  
Sensory Neurons ◽  
Reproductive Cycle ◽  
Neuronal Network ◽  
Nutrient Availability ◽  
Developmental Plasticity ◽  
State Dependent ◽  
Dauer Formation ◽  
Growth Promoting

Information about nutrient availability is assessed via largely unknown mechanisms to drive developmental decisions, including the choice of Caenorhabditis elegans larvae to enter into the reproductive cycle or the dauer stage. In this study, we show that CMK-1 CaMKI regulates the dauer decision as a function of feeding state. CMK-1 acts cell-autonomously in the ASI, and non cell-autonomously in the AWC, sensory neurons to regulate expression of the growth promoting daf-7 TGF-β and daf-28 insulin-like peptide (ILP) genes, respectively. Feeding state regulates dynamic subcellular localization of CMK-1, and CMK-1-dependent expression of anti-dauer ILP genes, in AWC. A food-regulated balance between anti-dauer ILP signals from AWC and pro-dauer signals regulates neuroendocrine signaling and dauer entry; disruption of this balance in cmk-1 mutants drives inappropriate dauer formation under well-fed conditions. These results identify mechanisms by which nutrient information is integrated in a small neuronal network to modulate neuroendocrine signaling and developmental plasticity.

scholarly journals Intergenerational Pathogen-Induced Diapause in Caenorhabditis elegans Is Modulated by mir-243

mBio ◽  
2020 ◽  
Vol 11 (5) ◽  
Author(s):  
Carolaing Gabaldón ◽  
Marcela Legüe ◽  
M. Fernanda Palominos ◽  
Lidia Verdugo ◽  
Florence Gutzwiller ◽  
...  
Keyword(s):  
Caenorhabditis Elegans ◽  
Noncoding Rna ◽  
Pathogenic Bacteria ◽  
Developmental Change ◽  
Differential Expression Analysis ◽  
Phenotypic Analysis ◽  
Content Type ◽  
C Elegans ◽  
Two Generations ◽  
Dauer Formation

ABSTRACT The interaction and communication between bacteria and their hosts modulate many aspects of animal physiology and behavior. Dauer entry as a response to chronic exposure to pathogenic bacteria in Caenorhabditis elegans is an example of a dramatic survival response. This response is dependent on the RNA interference (RNAi) machinery, suggesting the involvement of small RNAs (sRNAs) as effectors. Interestingly, dauer formation occurs after two generations of interaction with two unrelated moderately pathogenic bacteria. Therefore, we sought to discover the identity of C. elegans RNAs involved in pathogen-induced diapause. Using transcriptomics and differential expression analysis of coding and long and small noncoding RNAs, we found that mir-243-3p (the mature form of mir-243) is the only transcript continuously upregulated in animals exposed to both Pseudomonas aeruginosa and Salmonella enterica for two generations. Phenotypic analysis of mutants showed that mir-243 is required for dauer formation under pathogenesis but not under starvation. Moreover, DAF-16, a master regulator of defensive responses in the animal and required for dauer formation was found to be necessary for mir-243 expression. This work highlights the role of a small noncoding RNA in the intergenerational defensive response against pathogenic bacteria and interkingdom communication. IMPORTANCE Persistent infection of the bacterivore nematode C. elegans with bacteria such as P. aeruginosa and S. enterica makes the worm diapause or hibernate. By doing this, the worm closes its mouth, avoiding infection. This response takes two generations to be implemented. In this work, we looked for genes expressed upon infection that could mediate the worm diapause triggered by pathogens. We identify mir-243-3p as the only transcript commonly upregulated when animals feed on P. aeruginosa and S. enterica for two consecutive generations. Moreover, we demonstrate that mir-243-3p is required for pathogen-induced dauer formation, a new function that has not been previously described for this microRNA (miRNA). We also find that the transcriptional activators DAF-16, PQM-1, and CRH-2 are necessary for the expression of mir-243 under pathogenesis. Here we establish a relationship between a small RNA and a developmental change that ensures the survival of a percentage of the progeny.

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