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Histones Cause Aggregation and Fusion of Lipid Vesicles Containing Phosphatidylinositol-4-Phosphate

机译:组蛋白引起包含磷脂酰肌醇4-磷酸脂的脂质囊泡的聚集和融合

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摘要

In a previous article, we demonstrated that histones (H1 or histone octamers) interact with negatively charged bilayers and induce extensive aggregation of vesicles containing phosphatidylinositol-4-phosphate (PIP) and, to a lesser extent, vesicles containing phosphatidylinositol (PI). Here, we found that vesicles containing PIP, but not those containing PI, can undergo fusion induced by histones. Fusion was demonstrated through the observation of intervesicular mixing of total lipids and inner monolayer lipids, and by ultrastructural and confocal microscopy studies. Moreover, in both PI- and PIP-containing vesicles, histones caused permeabilization and release of vesicular aqueous contents, but the leakage mechanism was different (all-or-none for PI and graded release for PIP vesicles). These results indicate that histones could play a role in the remodeling of the nuclear envelope that takes place during the mitotic cycle.
机译:在上一篇文章中,我们证明了组蛋白(H1或组蛋白八聚体)与带负电荷的双层相互作用,并诱导了包含磷脂酰肌醇-4-磷酸酯(PIP)的囊泡的广泛聚集,并在较小程度上诱导了包含磷脂酰肌醇(PI)的囊泡的聚集。在这里,我们发现含有PIP但不含PI的囊泡可以经历组蛋白诱导的融合。通过观察总脂质和内部单层脂质的囊泡混合以及超微结构和共聚焦显微镜研究证明了融合。此外,在含有PI和PIP的囊泡中,组蛋白均引起囊泡含水量的渗透和释放,但渗漏机理不同(对于PI囊泡是全有或无,对于PIP囊泡是分级释放的)。这些结果表明,组蛋白可能在有丝分裂周期中发生的核膜重塑中起作用。

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