ArticleDevelopmental cell2019
CEH-60/PBX and UNC-62/MEIS Coordinate a Metabolic Switch that Supports Reproduction in C. elegans.
Article in Developmental cell, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed.
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- An mTORC2-Lipid Signaling Axis Controls Stress-Induced Organismal Death.Research square · 2026Article
- LIPL-1 and LIPL-2 are TCER-1-regulated lysosomal lipases with distinct roles in immunity and fertility.PLoS genetics · 2025Article
- Review
- SRS microscopy identifies inhibition of vitellogenesis as a mediator of lifespan extension by caloric restriction inbioRxiv : the preprint server for biology · 2025Article
- Non-cell-autonomous regulation of mTORC2 by Hedgehog signaling maintains lipid homeostasis.Cell reports · 2025Article
- Intestinal RICT-1 regulates the larval germline progenitor pool via the vitellogenin VIT-3 inbioRxiv : the preprint server for biology · 2025Article
- Loss of the vitellogenins confers a fitness disadvantage but does not impact brood size inmicroPublication biology · 2025Article
- Caffeine-Induced Upregulation ofNutrients · 2024Article
- ELO-6 expression predicts longevity in isogenic populations of Caenorhabditis elegans.Nature communications · 2024Article
- Kombucha Tea-associated microbes remodel host metabolic pathways to suppress lipid accumulation.PLoS genetics · 2024Article
- The F-box protein FBXL-5 governs vitellogenesis and lipid homeostasis inFrontiers in cell and developmental biology · 2024Article
- Opposing action of the FLR-2 glycoprotein hormone and DRL-1/FLR-4 MAP kinases balance p38-mediated growth and lipid homeostasis in C. elegans.PLoS biology · 2023Article
- An intestinal sphingolipid confers intergenerational neuroprotection.Nature cell biology · 2023Article
- Yolk-deprivedLife science alliance · 2023Article
- Article
- Vitellogenin accumulation leads to reproductive senescence by impairing lysosomal function.Science China. Life sciences · 2023Article
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Abstract
The molecular basis of how animals integrate metabolic, developmental, and environmental information before committing resources to reproduction is an unresolved issue in developmental biology. In C. elegans, adult animals reallocate fat stores from intestinal cells to the germline via low-density lipoprotein (LDL)-like particles to promote embryogenesis. Here, I demonstrate that two conserved homeodomain transcription factors, CEH-60/PBX and UNC-62/MEIS, coordinate a transcriptional network that supports reproduction while suppressing longevity and stress-response pathways. The CEH-60:UNC-62 heterodimer serves an unanticipated dual function in intestinal nuclei by directly activating the expression of lipoprotein genes while directly repressing stress-responsive genes. Consequently, ceh-60 mutants display fat storage defects, a dramatic lifespan extension, and hyper-activation of innate immunity genes. Finally, CEH-60 associates with PQM-1 at the DAF-16-associated element within the promoters of stress-responsive genes to control gene expression. Thus, CEH-60 governs an elaborate transcriptional network that balances stress responses and longevity against reproduction during developmental transitions.
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