The overall objective of the Caenorhabditis Genetics Center (CGC) is to promote research on the small metazoan Caenorhabditis elegans by acquiring, maintaining, and distributing genetically characterized nematode stocks. Researchers throughout the world use genetic stocks obtained from the CGC in diverse basic and applied research endeavors. Studies using this premier model organism have led to fundamental insights into basic biological mechanisms, including the genetic basis of programmed cell death, the discovery of microRNAs, and the mechanism of RNA interference in animals. The nematode has also proved important for understanding mechanisms of cancer progression and other diseases including Alzheimer's and Parkinson's, as well as for revealing basic mechanisms underlying human development. In addition, C. elegans serves as a key model for illuminating our understanding of parasitic nematodes with relevance to human and livestock health. As the sole general stock center for the nematode C. elegans, the CGC is an extremely important international research resource. The high demand for CGC strains reflects their great importance to the research community;currently more than 25,000 strains are distributed per year. The CGC curates C. elegans strains and distributes them upon request through an on-line ordering system. A new research component will be implemented to expand the activities of the CGC. The C. elegans genetic tool-kit will be enhanced through the generation of genetic tools to aid researchers in manipulations of lethal and sterile mutations.

Public Health Relevance

The Caenorhabditis Genetics Center (CGC) is the international repository and distribution center for the nematode C. elegans. Researchers throughout the world have used strains provided by the CGC to make important discoveries in diverse areas of biology, many with relevance to human health, including insights into neurodegenerative diseases, aging and cancer.

National Institute of Health (NIH)
Office of The Director, National Institutes of Health (OD)
Animal (Mammalian and Nonmammalian) Model, and Animal and Biological Material Resource Grants (P40)
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National Center for Research Resources Initial Review Group (RIRG)
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Chang, Michael
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University of Minnesota Twin Cities
Schools of Medicine
United States
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Jiang, Qiang; Li, Kai; Lu, Wen-Jing et al. (2018) Identification of small-molecule ion channel modulators in C. elegans channelopathy models. Nat Commun 9:3941
Kocsisova, Zuzana; Kornfeld, Kerry; Schedl, Tim (2018) Cell cycle accumulation of the proliferating cell nuclear antigen PCN-1 transitions from continuous in the adult germline to intermittent in the early embryo of C. elegans. BMC Dev Biol 18:12
Richman, Cory; Rashid, Sabih; Prashar, Shreya et al. (2018) C. elegans MANF Homolog Is Necessary for the Protection of Dopaminergic Neurons and ER Unfolded Protein Response. Front Neurosci 12:544
Koury, Emily; Harrell, Kailey; Smolikove, Sarit (2018) Differential RPA-1 and RAD-51 recruitment in vivo throughout the C. elegans germline, as revealed by laser microirradiation. Nucleic Acids Res 46:748-764
Leiteritz, Anne; Dilberger, Benjamin; Wenzel, Uwe et al. (2018) Betaine reduces ?-amyloid-induced paralysis through activation of cystathionine-?-synthase in an Alzheimer model of Caenorhabditis elegans. Genes Nutr 13:21
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Coleman, Brantley; Topalidou, Irini; Ailion, Michael (2018) Modulation of Gq-Rho Signaling by the ERK MAPK Pathway Controls Locomotion in Caenorhabditis elegans. Genetics 209:523-535
Morrison, Logan M; Edwards, Stacey L; Manning, Laura et al. (2018) Sentryn and SAD Kinase Link the Guided Transport and Capture of Dense Core Vesicles in Caenorhabditis elegans. Genetics 210:925-946
Martínez-Velázquez, Luis A; Ringstad, Niels (2018) Antagonistic regulation of trafficking to Caenorhabditis elegans sensory cilia by a Retinal Degeneration 3 homolog and retromer. Proc Natl Acad Sci U S A 115:E438-E447
Chisnell, Peter; Parenteau, T Richard; Tank, Elizabeth et al. (2018) The mTOR Target S6 Kinase Arrests Development in Caenorhabditis elegans When the Heat-Shock Transcription Factor Is Impaired. Genetics 210:999-1009

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