ArticleiScience2019
The Drosophila Chromodomain Protein Kismet Activates Steroid Hormone Receptor Transcription to Govern Axon Pruning and Memory In Vivo.
Article in iScience, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- Kismet/CHD7/CHD8 affects gut microbiota, mechanics, and the gut-brain axis in Drosophila melanogaster.Biophysical journal · 2025Article
- The CHD Protein, Kismet, Restricts Synaptic BMP Signaling at Glutamatergic Synapses.Neuroscience insights · 2025Article
- Kismet/CHD7/CHD8 and Amyloid Precursor Protein-like Regulate Synaptic Levels of Rab11 at theInternational journal of molecular sciences · 2024Article
- The CHD Protein Kismet Restricts the Synaptic Localization of Cell Adhesion Molecules at theInternational journal of molecular sciences · 2024Article
- Coregulators Reside withinInternational journal of molecular sciences · 2023Article
- Polycomb group genes are required for neuronal pruning in Drosophila.BMC biology · 2023Article
- The making of the Drosophila mushroom body.Frontiers in physiology · 2023Review
- The CHD8/CHD7/Kismet family links blood-brain barrier glia and serotonin to ASD-associated sleep defects.Science advances · 2021Article
- Nuclear receptors linking physiology and germline stem cells in Drosophila.Vitamins and hormones · 2021Review
- The CHD Protein, Kismet, is Important for the Recycling of Synaptic Vesicles during Endocytosis.Scientific reports · 2019Article
Corrections and comments
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Authors and funding
3 authors.
Funding
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Abstract
Axon pruning is critical for sculpting precise neural circuits. Although axon pruning has been described in the literature for decades, relatively little is known about the molecular and cellular mechanisms that govern axon pruning in vivo. Here, we show that the epigenetic reader Kismet (Kis) is required for developmental axon pruning in Drosophila mushroom bodies. Kis binds to cis-regulatory elements of the steroid hormone receptor ecdysone receptor (ecr) gene and is necessary for activating expression of EcR-B1. Kis promotes the active H3K36 di- and tri-methylation and H4K16 acetylation histone marks at the ecr locus. We show that transgenic EcR-B1 can rescue axon pruning and memory defects associated with loss of Kis and that the histone deacetylase inhibitor SAHA also rescues these phenotypes. EcR protein abundance is the cell-autonomous, rate-limiting step required to initiate axon pruning in Drosophila, and our data suggest this step is under the epigenetic control of Kis.
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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.