Riesen, Michèle, Feyst, Inna, Rattanavirotkul, Nattaphong, Ezcurra, Marina, Tullet, Jennifer M.A., Papatheodorou, Irene, Ziehm, Matthias, Au, Catherine, Gilliat, Ann F, Hellberg, Josephine, and others. (2014) MDL-1, a growth- and tumor-suppressor, slows aging and prevents germline hyperplasia and hypertrophy in C. elegans. Aging, 6 (2). pp. 98-117. E-ISSN 1945-4589. (The full text of this publication is not currently available from this repository. You may be able to access a copy if URLs are provided) (KAR id:43255)
The full text of this publication is not currently available from this repository. You may be able to access a copy if URLs are provided. |
Abstract
In C. elegans, increased lifespan in daf-2 insulin/IGF-1 receptor mutants is accompanied by up-regulation of the MDL-1 Mad basic helix-loop-helix leucine zipper transcription factor. Here we describe the role of mdl-1 in C. elegans germline proliferation and aging. The deletion allele mdl-1(tm311) shortened lifespan, and did so significantly more so in long-lived daf-2 mutants implying that mdl-1(+) contributes to effects of daf-2 on lifespan. mdl-1 mutant hermaphrodites also lay increased numbers of unfertilized oocytes. During aging, unfertilized oocytes in the uterus develop into tumors, whose development was accelerated by mdl-1(tm311). Opposite phenotypes were seen in daf-2 mutants, i.e. mdl-1 and daf-2 mutant germlines are hyperplastic and hypoplastic, respectively. Thus, MDL-1, like its mammalian orthologs, is an inhibitor of cell proliferation and growth that slows progression of an age-related pathology in C. elegans (uterine tumors). In addition, intestine-limited rescue of mdl-1 increased lifespan but not to wild type levels. Thus, mdl-1 likely acts both in the intestine and the germline to influence age-related mortality.
Item Type: | Article |
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Subjects: | Q Science > Q Science (General) |
Divisions: | Divisions > Division of Natural Sciences > Biosciences |
Depositing User: | Jennifer Tullet |
Date Deposited: | 13 Oct 2014 08:25 UTC |
Last Modified: | 05 Nov 2024 10:27 UTC |
Resource URI: | https://kar.kent.ac.uk/id/eprint/43255 (The current URI for this page, for reference purposes) |
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