scholarly journals The Developmental Timing Regulator hbl-1 Modulates the Dauer Formation Decision in Caenorhabditis elegans

Genetics ◽  
2010 ◽  
Vol 187 (1) ◽  
pp. 345-353 ◽  
Author(s):  
Xantha Karp ◽  
Victor Ambros
Keyword(s):  
Caenorhabditis Elegans ◽  
Developmental Timing ◽  
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.

scholarly journals Analysis of a lin-42/period Null Allele Implicates All Three Isoforms in Regulation of Caenorhabditis elegans Molting and Developmental Timing

2016 ◽  
Vol 6 (12) ◽  
pp. 4077-4086 ◽  
Author(s):  
Theresa L B Edelman ◽  
Katherine A McCulloch ◽  
Angela Barr ◽  
Christian Frøkjær-Jensen ◽  
Erik M Jorgensen ◽  
...  
Keyword(s):  
Caenorhabditis Elegans ◽  
Null Allele ◽  
Postembryonic Development ◽  
Developmental Timing ◽  
Critical Element ◽  
Coding Region ◽  
Protein Coding ◽  
Temporal Regulation ◽  
Larval Stages ◽  
Hypomorphic Alleles

Abstract The Caenorhabditis elegans heterochronic gene pathway regulates the relative timing of events during postembryonic development. lin-42, the worm homolog of the circadian clock gene, period, is a critical element of this pathway. lin-42 function has been defined by a set of hypomorphic alleles that cause precocious phenotypes, in which later developmental events, such as the terminal differentiation of hypodermal cells, occur too early. A subset of alleles also reveals a significant role for lin-42 in molting; larval stages are lengthened and ecdysis often fails in these mutant animals. lin-42 is a complex locus, encoding overlapping and nonoverlapping isoforms. Although existing alleles that affect subsets of isoforms have illuminated important and distinct roles for this gene in developmental timing, molting, and the decision to enter the alternative dauer state, it is essential to have a null allele to understand all of the roles of lin-42 and its individual isoforms. To remedy this problem and discover the null phenotype, we engineered an allele that deletes the entire lin-42 protein-coding region. lin-42 null mutants are homozygously viable, but have more severe phenotypes than observed in previously characterized hypomorphic alleles. We also provide additional evidence for this conclusion by using the null allele as a base for reintroducing different isoforms, showing that each isoform can provide heterochronic and molting pathway activities. Transcript levels of the nonoverlapping isoforms appear to be under coordinate temporal regulation, despite being driven by independent promoters. The lin-42 null allele will continue to be an important tool for dissecting the functions of lin-42 in molting and developmental timing.

The 21-nucleotide let-7 RNA regulates developmental timing in Caenorhabditis elegans

Nature ◽  
2000 ◽  
Vol 403 (6772) ◽  
pp. 901-906 ◽  
Author(s):  
Brenda J. Reinhart ◽  
Frank J. Slack ◽  
Michael Basson ◽  
Amy E. Pasquinelli ◽  
Jill C. Bettinger ◽  
...  
Keyword(s):  
Caenorhabditis Elegans ◽  
Developmental Timing

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.

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