ArticleCell death & disease2023
GEMC1 and MCIDAS interactions with SWI/SNF complexes regulate the multiciliated cell-specific transcriptional program.
Article in Cell death & disease, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 16 citations in OpenAlex.
- McIdas localizes to centrioles and controls centriole numbers through PLK4-dependent phosphorylation.EMBO reports · 2026Article
- Notch signaling stabilizes lengths of motile cilia in multiciliated cells in the lung.Life science alliance · 2026Article
- Unique clinical features and transcriptomic profiling of carcinogenesis in patients with familial lung cancer in Yunnan Province, Wumeng mountains, China.Respiratory research · 2026Article
- Ependymal and neural stem cells are close relatives.Stem cell reports · 2025Review
- Lineage trajectories and fate determinants of postnatal neural stem cells and ependymal cells in the developing ventricular zone.PLoS biology · 2025Article
- RBL2 represses the transcriptional activity of Multicilin to inhibit multiciliogenesis.Cell death & disease · 2024Article
- Formation and function of multiciliated cells.The Journal of cell biology · 2024Review
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Authors and funding
22 authors at 12 institutions in 8 countries.
Funding
Abstract
Multiciliated cells (MCCs) project dozens to hundreds of motile cilia from their apical surface to promote the movement of fluids or gametes in the mammalian brain, airway or reproductive organs. Differentiation of MCCs requires the sequential action of the Geminin family transcriptional activators, GEMC1 and MCIDAS, that both interact with E2F4/5-DP1. How these factors activate transcription and the extent to which they play redundant functions remains poorly understood. Here, we demonstrate that the transcriptional targets and proximal proteomes of GEMC1 and MCIDAS are highly similar. However, we identified distinct interactions with SWI/SNF subcomplexes; GEMC1 interacts primarily with the ARID1A containing BAF complex while MCIDAS interacts primarily with BRD9 containing ncBAF complexes. Treatment with a BRD9 inhibitor impaired MCIDAS-mediated activation of several target genes and compromised the MCC differentiation program in multiple cell based models. Our data suggest that the differential engagement of distinct SWI/SNF subcomplexes by GEMC1 and MCIDAS is required for MCC-specific transcriptional regulation and mediated by their distinct C-terminal domains.
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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.