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Cited by 171Genetics, Aging, and Longevity in Model OrganismsAutophagy in Disease and TherapyDevelopmental Biology and Gene Regulation

C. elegansfeeding defective mutants have shorter body lengths and increased autophagy

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Mörck, Catarina, Pilon, Marc·2006·BMC Developmental Biology
DOI 10.1186/1471-213x-6-39PMC PMC1559592
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Abstract

Background: Mutations that cause feeding defects in the nematode C. elegans are known to increase life span. Here we show that feeding defective mutants also have a second general trait in common, namely that they are small. Results: Our measurements of the body lengths of a variety of feeding defective mutants, or of a variety of double mutants affecting other pathways that regulate body length in C. elegans, i.e. the DBL-1/TGFβ, TAX-6/calcineurin and the SMA-1/β H-spectrin pathways, indicate that food uptake acts as a separate pathway regulating body length. In early stages, before eating begins, feeding defective worms have no defect in body length or, in some cases, have only slightly smaller body length compared to wild-type. A significant difference in body length is first noticeable at later larval stages, a difference that probably correlates with increasing starvation. We also show that autophagy is induced and that the quantity of fat is decreased in starved worms. Conclusion: Our results indicate that the long-term starvation seen in feeding-defective C. elegans mutants activates autophagy, and leads to depletion of fat deposits, small cell size and small body size.

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  • Studies in worms and flies support that functional macroautophagy is necessary to preserve normal lifespan.

    “studies by other groups in worms and flies seem to support that functional macroautophagy is necessary to preserve normal lifespan (Juhasz et al., 2007; Morck and Pilon, 2006; Simonsen et al., 2007)”

    From Protein Homeostasis and Aging: the importance of exquisite quality control (2011) · cites this paper as Morck and Pilon, 2006

    The Discussion (page unavailable) links increased autophagy in feeding-defective C. elegans mutants with increased longevity, but describes a role for autophagy in longevity as proposed. It does not show that functional autophagy is necessary to preserve normal lifespan. Its mention of flies in the Background concerns starvation-induced autophagy, not lifespan. (LLM, conf=0.84)

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Cited by

Sorted by citations

Authors
Mörck, C., & Pilon, M.
Affiliations
University of Gothenburg (SE)
Corresponding author
Pilon, Marc
ORCID
Pilon, Marc
Venue
BMC Developmental Biology
Publisher
Springer Science and Business Media LLC
Published
2006-08-03
Volume
6
Issue
1
Pages
39-39
ISSN
1471-213X (ISSN-L)
DOI
10.1186/1471-213x-6-39
PMC
PMC1559592
OpenAlex
W1533255176
Cited by
171
References
3
Citations by year
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FWCI
3.59
Type
journal article
Language
en
Open access
Licence
Locations
  • BMC Developmental Biology (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • Chalmers Publication Library (Chalmers University of Technology) (submittedVersion)
  • Chalmers Research (Chalmers University of Technology) (submittedVersion)
Funders
  • Cancerfonden
  • National Institutes of Health
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
  • Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Developmental Biology and Gene Regulation
Keywords
Caenorhabditis elegans, body length, autophagy, starvation, food uptake, fat deposition, cell size, longevity
MeSH terms
Animals, Autophagy, Feeding Behavior, Longevity, Mutation, Caenorhabditis elegans, Body Size

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