ArticleResearch square2026
Cooperative and Opposing Functions of ANP32E and VPS72 Govern Gene Promoter Chromatin Status.
Article in Research square, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Authors and funding
10 authors.
Funding
Abstract
The histone variant H2A.Z resides within active gene promoters, but how it influences chromatin state and nucleosome stability remains poorly understood. Here, we probe two H2A.Z binding proteins with seemingly opposing function: VPS72, an SRCAP subunit that aids in H2A.Z deposition, and ANP32E, a histone chaperone which is thought to remove H2A.Z. Using functional genomics and biochemical assays, we show that VPS72 and ANP32E co-occupy active promoters yet function antagonistically. VPS72 promotes H2A.Z incorporation, acetylation, BRG1 recruitment, and transcription, whereas ANP32E constrains these features by stabilizing nucleosomes. Loss of ANP32E increases VPS72 binding, chromatin accessibility, and transcription, while co-depletion of VPS72 reverses these effects. Reconstitution assays show that ANP32E promotes nucleosome assembly and prevents DNA unwrapping, providing a mechanistic basis for
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