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.
Thornton, Janet M,
and
Gems, David
(hide)
(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.
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(KAR id:43255)
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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.
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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.
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