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Peer-reviewedCC BY-NCNucleic acids research

HLH-30/TFEB is necessary for chromatin reorganization and maintenance of cell quiescence during starvation in C. elegans.

  • Marta Muñoz-Barrera1
  • Alejandro Mata-Cabana1
  • Almudena Moreno-Rivero1
  • Francine A Piubeli1
  • Beatriz Ren-Barroso1
  • Nada Al-Refaie2,3
  • Gabriel Gutierrez1
  • Daphne S Cabianca2
  • María Olmedo1
  1. 1Departamento de Genética, Facultad de Biología, Universidad de Sevilla, Seville 41012, Spain.
  2. 2Institute of Functional Epigenetics, Helmholtz Zentrum Muenchen, Neuherberg D-85764, Germany.
  3. 3Faculty of Medicine, Ludwig-Maximilians-Universität Muenchen, Munich D-80539, Germany.
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Abstract

Cellular quiescence is a low metabolic, non-proliferative state critical for tissue maintenance and regenerative capacity, with broad implications for aging and age-related diseases. In Caenorhabditis elegans, L1 developmental arrest upon hatching in the absence of food provides a robust in vivo model to study quiescence. Here, we investigate the roles of the transcription factors HLH-30/TFEB and DAF-16/FOXO during L1 arrest. We show that HLH-30 and DAF-16 collaborate to ensure survival under starvation, with reciprocal regulation of their subcellular localization and transcriptional activity. HLH-30 exerts broad transcriptional control during L1 arrest, modulating genes involved in chromosome organization and cell cycle progression. Profiling of chromatin spatial distribution reveals that HLH-30 is required for fasting-induced 3D chromatin reorganization. Loss of HLH-30 disrupts seam cell cycle arrest and causes the overactivation of the transcription factors BLMP-1 and CEBP-1, which contribute to premature initiation of developmental programs under starvation. Our findings uncover previously unrecognized functions of HLH-30 in genome architecture and quiescence regulation, highlighting conserved mechanisms of transcriptional control during nutrient deprivation with implications for aging and disease.

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Cite

BibTeXRIS
BibTeX
@article{munozbarrera2026hlh30tfeb,
  title = {{HLH-30/TFEB is necessary for chromatin reorganization and maintenance of cell quiescence during starvation in C. elegans.}},
  author = {Marta Muñoz-Barrera and Alejandro Mata-Cabana and Almudena Moreno-Rivero and Francine A Piubeli and Beatriz Ren-Barroso and Nada Al-Refaie and Gabriel Gutierrez and Daphne S Cabianca and María Olmedo},
  journal = {Nucleic acids research},
  year = {2026},
  month = sep,
  doi = {10.1093/nar/gkag949},
  url = {https://europepmc.org/article/MED/42847247},
  note = {CC BY-NC},
}
RIS
TY  - JOUR
TI  - HLH-30/TFEB is necessary for chromatin reorganization and maintenance of cell quiescence during starvation in C. elegans.
AU  - Marta Muñoz-Barrera
AU  - Alejandro Mata-Cabana
AU  - Almudena Moreno-Rivero
AU  - Francine A Piubeli
AU  - Beatriz Ren-Barroso
AU  - Nada Al-Refaie
AU  - Gabriel Gutierrez
AU  - Daphne S Cabianca
AU  - María Olmedo
PY  - 2026
DA  - 2026/09/01
JO  - Nucleic acids research
DO  - 10.1093/nar/gkag949
UR  - https://europepmc.org/article/MED/42847247
AB  - Cellular quiescence is a low metabolic, non-proliferative state critical for tissue maintenance and regenerative capacity, with broad implications for aging and age-related diseases. In Caenorhabditis elegans, L1 developmental arrest upon hatching in the absence of food provides a robust in vivo model to study quiescence. Here, we investigate the roles of the transcription factors HLH-30/TFEB and DAF-16/FOXO during L1 arrest. We show that HLH-30 and DAF-16 collaborate to ensure survival under starvation, with reciprocal regulation of their subcellular localization and transcriptional activity. HLH-30 exerts broad transcriptional control during L1 arrest, modulating genes involved in chromosome organization and cell cycle progression. Profiling of chromatin spatial distribution reveals that HLH-30 is required for fasting-induced 3D chromatin reorganization. Loss of HLH-30 disrupts seam cell cycle arrest and causes the overactivation of the transcription factors BLMP-1 and CEBP-1, which contribute to premature initiation of developmental programs under starvation. Our findings uncover previously unrecognized functions of HLH-30 in genome architecture and quiescence regulation, highlighting conserved mechanisms of transcriptional control during nutrient deprivation with implications for aging and disease.
SN  - 0305-1048
SN  - 1362-4962
ER  -