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MORC proteins regulate transcription factor binding by mediating chromatin compaction in active chromatin regions

BACKGROUND: The microrchidia (MORC) proteins are a family of evolutionarily conserved GHKL-type ATPases involved in chromatin compaction and gene silencing. Arabidopsis MORC proteins act in the RNA-directed DNA methylation (RdDM) pathway, where they act as molecular tethers to ensure the efficient e...

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Detalles Bibliográficos
Autores principales: Zhong, Zhenhui, Xue, Yan, Harris, C. Jake, Wang, Ming, Li, Zheng, Ke, Yunqing, Liu, Mukun, Zhou, Jessica, Jami-Alahmadi, Yasaman, Feng, Suhua, Wohlschlegel, James A., Jacobsen, Steven E.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10131428/
https://www.ncbi.nlm.nih.gov/pubmed/37101218
http://dx.doi.org/10.1186/s13059-023-02939-4
Descripción
Sumario:BACKGROUND: The microrchidia (MORC) proteins are a family of evolutionarily conserved GHKL-type ATPases involved in chromatin compaction and gene silencing. Arabidopsis MORC proteins act in the RNA-directed DNA methylation (RdDM) pathway, where they act as molecular tethers to ensure the efficient establishment of RdDM and de novo gene silencing. However, MORC proteins also have RdDM-independent functions although their underlying mechanisms are unknown. RESULTS: In this study, we examine MORC binding regions where RdDM does not occur in order to shed light on the RdDM-independent functions of MORC proteins. We find that MORC proteins compact chromatin and reduce DNA accessibility to transcription factors, thereby repressing gene expression. We also find that MORC-mediated repression of gene expression is particularly important under conditions of stress. MORC-regulated transcription factors can in some cases regulate their own transcription, resulting in feedback loops. CONCLUSIONS: Our findings provide insights into the molecular mechanisms of MORC-mediated chromatin compaction and transcription regulation. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s13059-023-02939-4.