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脂质堆积和胆固醇含量通过生物分子凝聚物调节膜的湿润和重塑。

Lipid packing and cholesterol content regulate membrane wetting and remodeling by biomolecular condensates.

作者信息

Mangiarotti Agustín, Sabri Elias, Schmidt Kita Valerie, Hoffmann Christian, Milovanovic Dragomir, Lipowsky Reinhard, Dimova Rumiana

机构信息

Max Planck Institute of Colloids and Interfaces, Science Park Golm, 14476, Potsdam, Germany.

Laboratory of Molecular Neuroscience, German Center for Neurodegenerative Diseases (DZNE), 10117, Berlin, Germany.

出版信息

Nat Commun. 2025 Mar 20;16(1):2756. doi: 10.1038/s41467-025-57985-2.

DOI:10.1038/s41467-025-57985-2
PMID:40113768
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11926106/
Abstract

Biomolecular condensates play a central role in cellular processes by interacting with membranes driving wetting transitions and inducing mutual remodeling. While condensates are known to locally alter membrane properties such as lipid packing and hydration, it remains unclear how membrane composition and phase state in turn affect condensate affinity. Here, we show that it is not only the membrane phase itself, but rather the degree of lipid packing that determines the condensate affinity for membranes. Increasing lipid chain length, saturation, or cholesterol content, enhances lipid packing, thereby decreasing condensate interaction. This regulatory mechanism is consistent across various condensate-membrane systems, highlighting the critical role of the membrane interface. In addition, protein adsorption promotes extensive membrane remodeling, including the formation of tubes and double-membrane sheets. Our findings reveal a mechanism by which membrane composition fine-tunes condensate wetting, highlighting its potential impact on cellular functions and organelle interactions.

摘要

生物分子凝聚物通过与膜相互作用驱动润湿转变并诱导相互重塑,在细胞过程中发挥核心作用。虽然已知凝聚物会局部改变膜的性质,如脂质堆积和水合作用,但膜组成和相态如何反过来影响凝聚物亲和力仍不清楚。在这里,我们表明决定凝聚物与膜亲和力的不仅是膜相本身,而是脂质堆积程度。增加脂质链长度、饱和度或胆固醇含量会增强脂质堆积,从而减少凝聚物相互作用。这种调节机制在各种凝聚物 - 膜系统中都是一致的,突出了膜界面的关键作用。此外,蛋白质吸附促进广泛的膜重塑,包括管和双膜片的形成。我们的研究结果揭示了一种膜组成微调凝聚物润湿性的机制,突出了其对细胞功能和细胞器相互作用的潜在影响。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0def/11926106/c9f45b7202b5/41467_2025_57985_Fig9_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0def/11926106/04e9da339067/41467_2025_57985_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0def/11926106/3bf9fc3bb3d3/41467_2025_57985_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0def/11926106/9207592096a1/41467_2025_57985_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0def/11926106/005e7939dba4/41467_2025_57985_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0def/11926106/13d36a44796a/41467_2025_57985_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0def/11926106/d085a69105a6/41467_2025_57985_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0def/11926106/450d4102d7cf/41467_2025_57985_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0def/11926106/f25bfbccbb7a/41467_2025_57985_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0def/11926106/c9f45b7202b5/41467_2025_57985_Fig9_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0def/11926106/04e9da339067/41467_2025_57985_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0def/11926106/3bf9fc3bb3d3/41467_2025_57985_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0def/11926106/9207592096a1/41467_2025_57985_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0def/11926106/005e7939dba4/41467_2025_57985_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0def/11926106/13d36a44796a/41467_2025_57985_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0def/11926106/d085a69105a6/41467_2025_57985_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0def/11926106/450d4102d7cf/41467_2025_57985_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0def/11926106/f25bfbccbb7a/41467_2025_57985_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0def/11926106/c9f45b7202b5/41467_2025_57985_Fig9_HTML.jpg

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