ArticleResearch square2026
Chromatin remodeling coordinates chromosome compaction, synaptonemal complex architecture and meiotic crossing-over.
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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13 authors.
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Abstract
Crossing-over between maternal and paternal chromosomes during meiosis relies on the maturation of recombination intermediates within the synaptonemal complex (SC). These events unfold within a hierarchically organized environment, in which linear arrays of chromatin loops are anchored to the axes of meiotic chromosomes. Yet, how chromatin organization is integrated with crossover maturation remains poorly understood. Here, we identify the nucleosome remodeler CHD1 as a previously unrecognized component of the mammalian SC. CHD1 localizes at the interface of synapsed homologs through direct interaction with the SC central-element protein SYCE1 and regulates meiotic chromosome organization. Conditional depletion of CHD1 in meiocytes increases chromatin accessibility at recombination hotspots, disrupts chromosome compaction, and reduces the spatial separation between homolog axes. These meiosis-specific structural defects are accompanied by impaired stabilization of crossover-promoting factors at incipient crossover sites. Together, our findings demonstrate that CHD1-mediated nucleosome remodeling shapes meiotic chromosome organization across scales, creating a chromatin environment that supports crossover maturation and fertility.
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