A simple method for maintaining large, aging populations of Caenorhabditis elegans

Gandhi, Sham Sunder; Santelli, John; Mitchell, David; Stiles, James W.; Sanadi, D.R.

doi:10.1016/0047-6374(80)90090-1

Cited by 120 publications

(97 citation statements)

References 17 publications

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“…Importantly, the reversibility and specificity of C22 makes it useful in the laboratory for other studies examining diverse aspects of the OET, as it can be used to stage embryos. Beyond this specific developmental stage, C22 can be used in studies such as aging assays, where it could serve as an alternative to FUDR treatment to block reproduction (Gandhi et al, 1980;Mitchell et al, 1979). FUDR can be problematic as it has been shown to artificially enhance lifespan in several mutant backgrounds (Aitlhadj and Stürzenbaum, 2010;Anderson et al, 2016;Davies et al, 2012;Van Raamsdonk and Hekimi, 2011).…”

Section: Discussionmentioning

confidence: 99%

A novel small molecule that disrupts a key event during the oocyte-to-embryo transition in C. elegans

et al. 2016

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The complex cellular events that occur in response to fertilization are essential for mediating the oocyte-to-embryo transition. Here, we describe a comprehensive small-molecule screen focused on identifying compounds that affect early embryonic events in Caenorhabditis elegans. We identify a single novel compound that disrupts early embryogenesis with remarkable stage and species specificity. The compound, named C22, primarily impairs eggshell integrity, leading to osmotic sensitivity and embryonic lethality. The C22-induced phenotype is dependent upon the upregulation of the LET-607/CREBH transcription factor and its candidate target genes, which primarily encode factors involved in diverse aspects of protein trafficking. Together, our data suggest that in the presence of C22, one or more key components of the eggshell are inappropriately processed, leading to permeable, inviable embryos. The remarkable specificity and reversibility of this compound will facilitate further investigation into the role and regulation of protein trafficking in the early embryo, as well as serve as a tool for manipulating the life cycle for other studies such as those involving aging.

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Section: Discussionmentioning

confidence: 99%

A novel small molecule that disrupts a key event during the oocyte-to-embryo transition in C. elegans

et al. 2016

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“…In measures of life span, day 0 is the L4 stage. In most trials, the inhibitor of DNA replication fluorodeoxyuridine (FUdR) was added to plates (Gandhi et al 1980) to prevent death due to internal hatching of eggs.…”

Section: Methodsmentioning

confidence: 99%

Clustering of Genetically Defined Allele Classes in the Caenorhabditis elegans DAF-2 Insulin/IGF-1 Receptor

Patel¹,

Garza-Garcia

Nanji³

et al. 2008

Genetics

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The DAF-2 insulin/IGF-1 receptor regulates development, metabolism, and aging in the nematode Caenorhabditis elegans. However, complex differences among daf-2 alleles complicate analysis of this gene. We have employed epistasis analysis, transcript profile analysis, mutant sequence analysis, and homology modeling of mutant receptors to understand this complexity. We define an allelic series of nonconditional daf-2 mutants, including nonsense and deletion alleles, and a putative null allele, m65. The most severe daf-2 alleles show incomplete suppression by daf-18(0) and daf-16(0) and have a range of effects on early development. Among weaker daf-2 alleles there exist distinct mutant classes that differ in epistatic interactions with mutations in other genes. Mutant sequence analysis (including 11 newly sequenced alleles) reveals that class 1 mutant lesions lie only in certain extracellular regions of the receptor, while class 2 (pleiotropic) and nonconditional missense mutants have lesions only in the ligand-binding pocket of the receptor ectodomain or the tyrosine kinase domain. Effects of equivalent mutations on the human insulin receptor suggest an altered balance of intracellular signaling in class 2 alleles. These studies consolidate and extend our understanding of the complex genetics of daf-2 and its underlying molecular biology.

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“…Development of uterine masses can be suppressed by feeding worms with fluorodeoxyuridine (FUdR), which blocks DNA replication. However, FUdR administration does not usually increase C. elegans lifespan (14), implying that these uterine growths do not contribute to mortality. More broadly, age changes in the gonad seem not to have major effects on organismal aging, since removal of the entire gonad does not increase lifespan, at least not in wild-type fully fed animals (25,58).…”

Section: Aging In the Uterusmentioning

confidence: 99%

Alternative Perspectives on Aging inCaenorhabditis elegans: Reactive Oxygen Species or Hyperfunction?

Gems

Guardia

2013

Antioxidants & Redox Signaling

155

122

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Significance: The biological mechanisms at the heart of the aging process are a long-standing mystery. An influential theory has it that aging is the result of an accumulation of molecular damage, caused in particular by reactive oxygen species produced by mitochondria. This theory also predicts that processes that protect against oxidative damage (involving detoxification, repair, and turnover) protect against aging and increase lifespan. Recent Advances: However, recent tests of the oxidative damage theory, many using the short-lived nematode worm Caenorhabditis elegans, have often failed to support the theory. This motivates consideration of alternative models. One new theory, conceived by M.V. Blagosklonny, proposes that aging is caused by hyperfunction, that is, overactivity during adulthood of processes (particularly biosynthetic) that contribute to development and reproduction. Such hyperfunction can lead to hypertrophy-associated pathologies, which cause the age increase in death. Critical Issues: Here we assess whether the hyperfunction theory is at all consistent with what is known about C. elegans aging, and conclude that it is. In particular, during adulthood, C. elegans shows a number of changes that may reflect pathology and/or hyperfunction. Such changes seem to contribute to death, at least in some cases (e.g., yolk accumulation). Future Directions: Our assessment suggests that the hyperfunction theory is a plausible alternative to the molecular damage theory to explain aging in C. elegans. Antioxid. Redox Signal. 19, 321-329.

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A simple method for maintaining large, aging populations of Caenorhabditis elegans

Cited by 120 publications

References 17 publications

A novel small molecule that disrupts a key event during the oocyte-to-embryo transition in C. elegans

A novel small molecule that disrupts a key event during the oocyte-to-embryo transition in C. elegans

Clustering of Genetically Defined Allele Classes in the Caenorhabditis elegans DAF-2 Insulin/IGF-1 Receptor

Alternative Perspectives on Aging inCaenorhabditis elegans: Reactive Oxygen Species or Hyperfunction?

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