The INO80 chromatin remodeling complex plays a critical role in shaping the dynamic chromatin environment. The diverse functions of the evolutionarily conserved INO80 complex have been widely reported. However, the role of INO80 in modulating the histone variant H2A.Z is controversial. Moreover, whether INO80 helps regulate heterochromatin remains unknown. Here, we characterize the regulatory effects of OsINO80 on protein-coding genes and transposable elements (TEs) in rice. Upon OsINO80 overexpression in rice, we found three types of OsINO80-occupied regions with different chromatin signatures: type I (enriched with H2A.Z), type II (enriched with H3K9me2), and type III (deficient in H2A.Z/H3K9me2). Loss of OsINO80 results in a decrease in H3K27me3, but not H2A.Z, at type I regions as well as a decrease in H3K9me2 at type II regions, which correlates with TE activation and transposition. Our findings reveal that OsINO80 facilitates H3K27me3 establishment, promotes H3K9me2 deposition, and maintains TE silencing.
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http://dx.doi.org/10.1038/s41467-024-55387-4 | DOI Listing |
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11686384 | PMC |
Clin Rev Allergy Immunol
December 2024
Department of Dermatology, Second Affiliated Hospital, Zhejiang University School of Medicine, 88 Jiefang Road, Hangzhou, 310009, People's Republic of China.
The switch/sucrose non-fermentable (SWI/SNF) chromatin remodeling complexes (also referred to as BAF complexes) are composed of multiple subunits, which regulate the nucleosome translocation and chromatin accessibility. In recent years, significant advancements have been made in understanding mutated genes encoding subunits of the SWI/SNF complexes in cancer biology. Nevertheless, the role of SWI/SNF complexes in immune response and inflammatory diseases continues to attract significant attention.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
NYU Grossman School of Medicine, New York, NY, USA.
Background: Down syndrome (DS) is strongly associated with Alzheimer's disease (AD), attributable to APP overexpression, displaying common features with early-onset AD (EOAD) and late-onset AD (LOAD) like Amyloid-β (Aβ) and tau pathology. Here, we evaluated the Aβ plaques proteome of DS, EOAD and LOAD.
Method: We used unbiased localized proteomics to analyze amyloid plaques and the adjacent plaque-devoid tissue ('AD non-plaque') from post-mortem paraffin-embedded tissues in three subtypes of AD (n = 20/group): DS (59.
Alzheimers Dement
December 2024
Department of Neurology, Columbia University, New York, NY, USA.
Background: While dysregulated local innate immunity and microglial dysfunction are thought to play a pathogenic role in Alzheimer's disease (AD), the underlying mechanisms remain unclear. Importantly, activation of immune and metabolic pathways in myeloid cells can lead to a functional reprogramming process, termed innate immune memory (IIM), in which the response to an initial stimulus shapes long-lasting epigenetic modifications that alter the response to future inflammatory stimuli. This epigenetic imprinting process has been minimally studied in microglia.
View Article and Find Full Text PDFNat Cardiovasc Res
January 2025
Hubrecht Institute, Royal Netherlands Academy of Arts and Sciences (KNAW) and University Medical Center Utrecht, Utrecht, The Netherlands.
In contrast to adult mammalian hearts, the adult zebrafish heart efficiently replaces cardiomyocytes lost after injury. Here we reveal shared and species-specific injury response pathways and a correlation between Hmga1, an architectural non-histone protein, and regenerative capacity, as Hmga1 is required and sufficient to induce cardiomyocyte proliferation and required for heart regeneration. In addition, Hmga1 was shown to reactivate developmentally silenced genes, likely through modulation of H3K27me3 levels, poising them for a pro-regenerative gene program.
View Article and Find Full Text PDFNat Commun
January 2025
Goethe University Frankfurt, Institute for Cardiovascular Physiology, Frankfurt, Germany.
The coordination of chromatin remodeling is essential for DNA accessibility and gene expression control. The highly conserved and ubiquitously expressed SWItch/Sucrose Non-Fermentable (SWI/SNF) chromatin remodeling complex plays a central role in cell type- and context-dependent gene expression. Despite the absence of a defined DNA recognition motif, SWI/SNF binds lineage specific enhancers genome-wide where it actively maintains open chromatin state.
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