Histone Chaperone Deficiency in Arabidopsis Plants Triggers Adaptive Epigenetic Changes in Histone Variants and Modifications

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Publikace nespadá pod Pedagogickou fakultu, ale pod Středoevropský technologický institut. Oficiální stránka publikace je na webu muni.cz.
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FRANEK Michal NEŠPOR DADEJOVÁ Martina PÍREK Pavlína KRYŠTOFOVÁ Karolína DOBISOVÁ Tereza ZDRÁHAL Zbyněk DVOŘÁČKOVÁ Martina LOCHMANOVÁ Gabriela

Rok publikování 2024
Druh Článek v odborném periodiku
Fakulta / Pracoviště MU

Středoevropský technologický institut

Citace
www https://www.mcponline.org/article/S1535-9476(24)00085-9/fulltext
Doi http://dx.doi.org/10.1016/j.mcpro.2024.100795
Klíčová slova Arabidopsis; chromatin remodeling; histone chaperone complex; histone variants; immunochemistry; mass spectrometry; post-translational modifications
Popis At the molecular scale, adaptive advantages during plant growth and development rely on modulation of gene expression, primarily provided by epigenetic machinery. One crucial part of this machinery is histone posttranslational modifications, which form a flexible system, driving transient changes in chromatin, and defining particular epigenetic states. Posttranslational modifications work in concert with replication-independent histone variants further adapted for transcriptional regulation and chromatin repair. However, little is known about how such complex regulatory pathways are orchestrated and interconnected in cells. In this work, we demonstrate the utility of mass spectrometry-based approaches to explore how different epigenetic layers interact in Arabidopsis mutants lacking certain histone chaperones. We show that defects in histone chaperone function (e.g., chromatin assembly factor-1 or nucleosome assembly protein 1 mutations) translate into an altered epigenetic landscape, which aids the plant in mitigating internal instability. We observe changes in both the levels and distribution of H2A.W.7, altogether with partial repurposing of H3.3 and changes in the key repressive (H3K27me1/2) or euchromatic marks (H3K36me1/2). These shifts in the epigenetic profile serve as a compensatory mechanism in response to impaired integration of the H3.1 histone in the fas1 mutants. Altogether, our findings suggest that maintaining genome stability involves a two-tiered approach. The first relies on flexible adjustments in histone marks, while the second level requires the assistance of chaperones for histone variant replacement.
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