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偏倚性组蛋白 H3 核小体驱逐引发. 的生物膜生长。

Biased eviction of variant histone H3 nucleosomes triggers biofilm growth in .

机构信息

Molecular Mycology Laboratory, Molecular Biology and Genetics Unit, Jawaharlal Nehru Centre for Advanced Scientific Research , Bangalore, Karnataka, India.

出版信息

mBio. 2023 Oct 31;14(5):e0206323. doi: 10.1128/mbio.02063-23. Epub 2023 Sep 28.

DOI:10.1128/mbio.02063-23
PMID:37768046
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10653867/
Abstract

lives as a commensal in most healthy humans but can cause superficial skin infections to life-threatening systemic infections. 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 . In this study, we addressed how a variant histone H3V, a previously identified negative regulator of biofilm formation, modulates gene expression changes. By providing compelling evidence, we show that biased eviction of H3V 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 , a medically relevant pathogen.

摘要

在大多数健康人类中作为共生菌生活,但也可能导致从浅表皮肤感染到危及生命的全身感染。 还会在生物和非生物表面形成生物膜。生物膜细胞难以治疗,并且对抗真菌药物高度耐药。与浮游细胞相比,生物膜细胞中差异调节了一组特定的基因。在这项研究中,我们研究了一种变体组蛋白 H3V(先前被鉴定为生物膜形成的负调节剂)如何调节基因表达变化。通过提供令人信服的证据,我们表明,在生物膜相关基因的启动子处,H3V 核小体的偏向性排出有利于转录激活剂和抑制剂对基因表达的调节。我们的研究是对浮游和生物膜状态下全基因组核小体占有率的全面研究,揭示了在医学相关病原体中,生物膜生长模式下向开放染色质景观的转变。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b4b1/10653867/a77b7e0e9354/mbio.02063-23.f006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b4b1/10653867/7ed560a1df51/mbio.02063-23.f001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b4b1/10653867/9db9748fd314/mbio.02063-23.f002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b4b1/10653867/cfa3d8d74a4a/mbio.02063-23.f003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b4b1/10653867/57fceb631362/mbio.02063-23.f004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b4b1/10653867/e15b71be2c92/mbio.02063-23.f005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b4b1/10653867/a77b7e0e9354/mbio.02063-23.f006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b4b1/10653867/7ed560a1df51/mbio.02063-23.f001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b4b1/10653867/9db9748fd314/mbio.02063-23.f002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b4b1/10653867/cfa3d8d74a4a/mbio.02063-23.f003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b4b1/10653867/57fceb631362/mbio.02063-23.f004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b4b1/10653867/e15b71be2c92/mbio.02063-23.f005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b4b1/10653867/a77b7e0e9354/mbio.02063-23.f006.jpg

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