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膜流动性在原始细胞增殖中的关键作用。

Crucial role for membrane fluidity in proliferation of primitive cells.

机构信息

Centre for Bacterial Cell Biology, Institute for Cell and Molecular Biosciences, The Medical School, Newcastle University, Newcastle upon Tyne NE2 4HH, UK.

出版信息

Cell Rep. 2012 May 31;1(5):417-23. doi: 10.1016/j.celrep.2012.03.008. Epub 2012 Apr 26.

Abstract

The cell wall is a defining structural feature of the bacterial subkingdom. However, most bacteria are capable of mutating into a cell-wall-deficient "L-form" state, requiring remarkable physiological and structural adaptations. L-forms proliferate by an unusual membrane deformation and scission process that is independent of the conserved and normally essential FtsZ based division machinery, and which may provide a model for the replication of primitive cells. Candidate gene screening revealed no requirement for the cytoskeletal systems that might actively drive membrane deformation or scission. Instead, we uncovered a crucial role for branched-chain fatty acid (BCFA) synthesis. BCFA-deficient mutants grow and undergo pulsating shape changes, but membrane scission fails, abolishing the separation of progeny cells. The failure in scission is associated with a reduction in membrane fluidity. The results identify a step in L-form proliferation and demonstrate that purely biophysical processes may have been sufficient for proliferation of primitive cells.

摘要

细胞壁是细菌亚界的一个定义性结构特征。然而,大多数细菌能够突变为细胞壁缺陷的“L 型”状态,需要显著的生理和结构适应。L 型通过一种不寻常的膜变形和分裂过程增殖,该过程独立于保守且通常必不可少的基于 FtsZ 的分裂机制,并且可能为原始细胞的复制提供模型。候选基因筛选未发现对可能主动驱动膜变形或分裂的细胞骨架系统的需求。相反,我们发现支链脂肪酸 (BCFA) 合成的关键作用。BCFA 缺陷突变体生长并经历脉动形状变化,但膜分裂失败,阻止了后代细胞的分离。分裂失败与膜流动性降低有关。结果确定了 L 型增殖的一个步骤,并证明纯粹的物理过程可能足以促进原始细胞的增殖。

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