ArticleProceedings of the National Academy of Sciences of the United States of America2014
The Caenorhabditis elegans HP1 family protein HPL-2 maintains ER homeostasis through the UPR and hormesis.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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23 citing papers in PubMed, 45 citations in OpenAlex.
- RNA exosome-driven RNA processing instructs the duration of the unfolded protein response.Nucleic acids research · 2025Article
- Redox regulation of UPR signalling and mitochondrial ER contact sites.Cellular and molecular life sciences : CMLS · 2024Review
- Article
- Dithiothreitol causes toxicity ineLife · 2022Article
- Stress Responses as Master Keys to Epigenomic Changes in Transcriptome and Metabolome for Cancer Etiology and Therapeutics.Molecular and cellular biology · 2022Article
- Hijacking Cellular Stress Responses to Promote Lifespan.Frontiers in aging · 2022Review
- The roles of inducible chromatin and transcriptional memory in cellular defense system responses to redox-active pollutants.Free radical biology & medicine · 2021Review
- Auxin confers protection against ER stress inBiology open · 2021Article
- Endoplasmic Reticulum Homeostasis and Stress Responses in Caenorhabditis elegans.Progress in molecular and subcellular biology · 2021Article
- Telomerase reverse transcriptase downregulation by RNA interference modulates endoplasmic reticulum stress and mitochondrial energy production.Molecular biology reports · 2020Article
- Molecular Effects of Silver Nanoparticles on Monogenean Parasites: Lessons fromInternational journal of molecular sciences · 2020Article
- Beyond the cell factory: Homeostatic regulation of and by the UPRScience advances · 2020Review
- MANF deletion abrogates early larval Caenorhabditis elegans stress response to tunicamycin and Pseudomonas aeruginosa.European journal of cell biology · 2019Article
- Dietary restriction improves proteostasis and increases life span through endoplasmic reticulum hormesis.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Nuclear Organization in Stress and Aging.Cells · 2019Review
- Methods to Determine the Role of Autophagy Proteins in C. elegans Aging.Methods in molecular biology (Clifton, N.J.) · 2019Article
- Review
- Endoplasmic reticulum proteostasis impairment in aging.Aging cell · 2017Review
- Differential adiponectin signalling couples ER stress with lipid metabolism to modulate ageing in C. elegans.Scientific reports · 2017Article
- Adaptive preconditioning in neurological diseases - therapeutic insights from proteostatic perturbations.Brain research · 2016Review
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cellular adaptation to environmental changes and stress relies on a wide range of regulatory mechanisms that are tightly controlled at several levels, including transcription. Chromatin structure and chromatin binding proteins are important factors contributing to the transcriptional response to stress. However, it remains largely unknown to what extent specific chromatin factors influence the response to distinct forms of stress in a developmental context. One of the best characterized stress response pathways is the unfolded protein response (UPR), which is activated by accumulation of misfolded proteins in the endoplasmic reticulum (ER). Here, we show that Caenorhabditis elegans heterochromatin protein like-2 (HPL-2), the homolog of heterochromatin protein 1 (HP1), down-regulates the UPR in the intestine. Inactivation of HPL-2 results in an enhanced resistance to ER stress dependent on the X-box binding protein 1 (XBP-1)/inositol requiring enzyme 1 branch of the UPR and the closely related process of autophagy. Increased resistance to ER stress in animals lacking HPL-2 is associated with increased basal levels of XBP-1 activation and ER chaperone expression under physiological conditions, which may in turn activate an adaptive response known as ER hormesis. HPL-2 expression in intestinal cells is sufficient to rescue stress resistance, whereas expression in neuronal cells negatively influenced the ER stress response through a cell-nonautonomous mechanism. We further show that the retinoblastoma protein homolog LIN-35 and the LIN-13 zinc finger protein act in the same pathway as HPL-2 to limit the ER stress response. Altogether, our results point to multiple functions for HP1 in different cell types to maintain ER homeostasis.
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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.