ArticleMechanisms of development2016
Loss of histone deacetylase HDAC1 induces cell death in Drosophila epithelial cells through JNK and Hippo signaling.
Article in Mechanisms of development, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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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
8 citing papers in PubMed, 9 citations in OpenAlex.
- Class I histone deacetylases and their inhibitors as targets to modulate cellular senescence in osteoarthritis.GeroScience · 2026Article
- Reversible acetylation of Hpo regulates the Hippo pathway.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Schlank orchestrates insect developmental transition by switching H3K27 acetylation to trimethylation in the prothoracic gland.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Genome-Wide Expression Analysis of Long Noncoding RNAs and Their Target Genes in MetafemaleInternational journal of molecular sciences · 2023Article
- EGFR phosphorylates HDAC1 to regulate its expression and anti-apoptotic function.Cell death & disease · 2021Article
- The histone deacetylase NlHDAC1 regulates both female and male fertility in the brown planthopper, Nilaparvata lugens.Open biology · 2018Article
- The histone deacetylase HDAC1 positively regulates Notch signaling duringBiology open · 2018Article
- APLP2 Modulates JNK-Dependent Cell Migration inBioMed research international · 2018Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Inactivation of HDAC1 and its homolog HDAC2 or addition of HDAC inhibitors in mammalian systems induces apoptosis, cell cycle arrest, and developmental defects. Although these phenotypes have been extensively characterized, the precise underlying mechanisms remain unclear, particularly in in vivo settings. In this study, we show that inactivation of Rpd3, the only HDAC1 and HDAC2 ortholog in Drosophila, induced apoptosis and clone elimination in the developing eye and wing imaginal discs. Depletion of Rpd3 by RNAi cell-autonomously increased JNK activities and decreased activities of Yki, the nuclear effecter of Hippo signaling pathway. In addition, inhibition of JNK activities largely rescued Rpd3 RNAi-induced apoptosis, but did not affect its inhibition of Yki activities. Conversely, increasing the Yki activities largely rescued Rpd3 RNAi-induced apoptosis, but did not affect its induction of JNK activities. Furthermore, inactivation of Mi-2, a core component of the Rpd3-containing NuRD complex strongly induced JNK activities; while inactivation of Sin3A, a key component of the Rpd3-containing Sin3 complex, significantly inhibited Yki activities. Taken together, these results reveal that inactivation of Rpd3 independently regulates JNK and Yki activities and that both Hippo and JNK signaling pathways contribute to Rpd3 RNAi-induced apoptosis.
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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.