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On biotic and abiotic surfaces, the planktonic free-floating yeast cells often form biofilms, a multi-drug-resistant three-dimensional community of yeast and filamentous cells. While alterations in gene expression patterns during planktonic to biofilm growth transitions in\n            <jats:italic>C. albicans<\/jats:italic>\n            have been studied, the underlying molecular mechanisms largely remain unexplored. Previously, we identified a histone H3 variant (H3V\n            <jats:sup>CTG<\/jats:sup>\n            ), which acts as a negative regulator of biofilm growth in\n            <jats:italic>C. albicans<\/jats:italic>\n            . In the current study, we performed genome-wide profiling of H3V\n            <jats:sup>CTG<\/jats:sup>\n            nucleosomes in\n            <jats:italic>C. albicans<\/jats:italic>\n            planktonic cells and found them to be enriched at promoter regions. In planktonic cells, H3V\n            <jats:sup>CTG<\/jats:sup>\n            -enriched regions are mostly devoid of histone H3 post-translational modifications that allow active transcription, thus strengthening the role of H3V\n            <jats:sup>CTG<\/jats:sup>\n            as a negative regulator of biofilm formation. By combining genome-wide transcriptional alterations, nucleosome positioning (MNase-seq), and DNA accessibility (ATAC-seq) assays, we show a significant reduction in the total number of nucleosomes in biofilm cells as compared to planktonic cells indicating a more open chromatin state during biofilm growth. Finally, we propose that H3V\n            <jats:sup>CTG<\/jats:sup>\n            -nucleosome eviction at promoters of biofilm-relevant genes in biofilm-grown cells contributes to achieve the open chromatin state by facilitating easy promoter access of master regulators (activators and repressors) for modulation of gene expression observed during growth phase transitions.\n          <\/jats:p>\n          <jats:sec>\n            <jats:title>IMPORTANCE<\/jats:title>\n            <jats:p>\n              <jats:italic>Candida albicans<\/jats:italic>\n              lives as a commensal in most healthy humans but can cause superficial skin infections to life-threatening systemic infections.\n              <jats:italic>C. albicans<\/jats:italic>\n              also forms biofilms on biotic and abiotic surfaces. Biofilm cells are difficult to treat and highly resistant to antifungals. A specific set of genes is differentially regulated in biofilm cells as compared to free-floating planktonic cells of\n              <jats:italic>C. albicans<\/jats:italic>\n              . In this study, we addressed how a variant histone H3V\n              <jats:sup>CTG<\/jats:sup>\n              , a previously identified negative regulator of biofilm formation, modulates gene expression changes. By providing compelling evidence, we show that biased eviction of H3V\n              <jats:sup>CTG<\/jats:sup>\n              nucleosomes at the promoters of biofilm-relevant genes facilitates the accessibility of both transcription activators and repressors to modulate gene expression. Our study is a comprehensive investigation of genome-wide nucleosome occupancy in both planktonic and biofilm states, which reveals transition to an open chromatin landscape during biofilm mode of growth in\n              <jats:italic>C. albicans<\/jats:italic>\n              , a medically relevant pathogen.\n            <\/jats:p>\n          <\/jats:sec>","DOI":"10.1128\/mbio.02063-23","type":"journal-article","created":{"date-parts":[[2023,9,28]],"date-time":"2023-09-28T13:01:51Z","timestamp":1695906111000},"update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":5,"title":["Biased eviction of variant histone H3 nucleosomes triggers biofilm growth in\n            <i>Candida albicans<\/i>"],"prefix":"10.1128","volume":"14","author":[{"ORCID":"https:\/\/orcid.org\/0009-0002-0376-8667","authenticated-orcid":false,"given":"Priya","family":"Brahma","sequence":"first","affiliation":[{"name":"Molecular Mycology Laboratory, 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