ArticleAging2014
MDL-1, a growth- and tumor-suppressor, slows aging and prevents germline hyperplasia and hypertrophy in C. elegans.
Article in Aging, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
23 citing papers in PubMed, 35 citations in OpenAlex.
- Scavenger Cells Failure to Maintain Systemic RNA Homeostasis Causes Epigenetically Inherited Germline Tumors.bioRxiv : the preprint server for biology · 2026Article
- Machine learning predicts lifespan and suggests underlying causes of death in aging C. elegans.Communications biology · 2025Article
- A hierarchy of causes of death in senescentbioRxiv : the preprint server for biology · 2025Article
- Characterization of Effects of mTOR Inhibitors on Aging in Caenorhabditis elegans.The journals of gerontology. Series A, Biological sciences and medical sciences · 2024Article
- ConsideringCells · 2024Review
- C. elegans ageing is accelerated by a self-destructive reproductive programme.Nature communications · 2023Article
- Article
- Immunity-longevity tradeoff neurally controlled by GABAergic transcription factor PITX1/UNC-30.Cell reports · 2021Article
- C. elegans Eats Its Own Intestine to Make Yolk Leading to Multiple Senescent Pathologies.Current biology : CB · 2018Article
- Article
- Article
- A parthenogenetic quasi-program causes teratoma-like tumors during aging in wild-typeNPJ aging and mechanisms of disease · 2018Article
- Two forms of death in ageing Caenorhabditis elegans.Nature communications · 2017Article
- MicroRNA mir-34 provides robustness to environmental stress response via the DAF-16 network in C. elegans.Scientific reports · 2016Article
- Microsporidia Intracellular Development Relies on Myc Interaction Network Transcription Factors in the Host.G3 (Bethesda, Md.) · 2016Article
- Article
- Mondo complexes regulate TFEB via TOR inhibition to promote longevity in response to gonadal signals.Nature communications · 2016Article
- Reproductive Aging Drives Protein Accumulation in the Uterus and Limits Lifespan in C. elegans.PLoS genetics · 2015Article
- HES-Mediated Repression of Pten in Caenorhabditis elegans.G3 (Bethesda, Md.) · 2015Article
- Longevity Genes Revealed by Integrative Analysis of Isoform-Specific daf-16/FoxO Mutants of Caenorhabditis elegans.Genetics · 2015Article
Corrections and comments
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Authors and funding
12 authors at 4 institutions in 1 country.
Funding
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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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.