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马达蛋白对离子通量的控制是胚胎左右不对称发育的早期步骤。

Motor protein control of ion flux is an early step in embryonic left-right asymmetry.

作者信息

Levin Michael

机构信息

Cytokine Biology Department, The Forsyth Institute and Department of Craniofacial and Developmental Biology, Harvard School of Dental Medicine, Boston, MA, USA.

出版信息

Bioessays. 2003 Oct;25(10):1002-10. doi: 10.1002/bies.10339.

DOI:10.1002/bies.10339
PMID:14505367
Abstract

The invariant left-right asymmetry of animal body plans raises fascinating questions in cell, developmental, evolutionary, and neuro-biology. While intermediate mechanisms (e.g., asymmetric gene expression) have been well-characterized, very early steps remain elusive. Recent studies suggested a candidate for the origins of asymmetry: rotary movement of extracellular morphogens by cilia during gastrulation. This model is intellectually satisfying, because it bootstraps asymmetry from the intrinsic biochemical chirality of cilia. However, conceptual and practical problems remain with this hypothesis, and the genetic data is consistent with a different mechanism. Based on wide-ranging data on ion fluxes and motor protein action in a number of species, a model is proposed whereby laterality is generated much earlier, by asymmetric transport of ions, which results in pH/voltage gradients across the midline. These asymmetries are in turn generated by a new candidate for "step 1": asymmetric localization of electrogenic proteins by cytoplasmic motors.

摘要

动物身体结构的左右不对称性在细胞生物学、发育生物学、进化生物学和神经生物学中引发了诸多引人入胜的问题。尽管中间机制(如不对称基因表达)已得到充分表征,但非常早期的步骤仍不清楚。最近的研究提出了一个不对称起源的候选因素:原肠胚形成期间纤毛对细胞外形态发生素的旋转运动。这个模型在理论上令人满意,因为它从纤毛固有的生化手性中产生了不对称性。然而,这个假设仍然存在概念和实际问题,并且遗传数据与另一种机制一致。基于对多个物种中离子通量和运动蛋白作用的广泛数据,提出了一个模型,即通过离子的不对称运输更早地产生左右不对称性,这会导致中线两侧的pH/电压梯度。这些不对称性反过来由“第一步”的一个新候选因素产生:细胞质马达对产电蛋白的不对称定位。

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Bioessays. 2003 Oct;25(10):1002-10. doi: 10.1002/bies.10339.
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