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5.9 结论

目前收集的数据表明,某些细胞机制参与了硅藻形态发生的控制。一般情况如下所示。首先,在细胞被肌动蛋白丝环隔开后 [56] ,微管中心向形成SDV的位置移动以控制其对称性。SDV的起源仍有争议,但它与微管中心的联系似乎在形态发生的起始中起着重要作用。在形态发生的某些阶段,细胞骨架(具有微管网络和肌动蛋白丝的微管中心)通过其成分的相互作用来控制SDV的准确位置、形成瓣膜的形状,以及可能的精细结构。SDV由可能依赖于微管的囊泡运输提供 [61] 。微管还可以确定水通道蛋白分子的特定模式,这些模式可以去除二氧化硅聚合产生的多余水分 [74] ,或控制参与硅化作用的其他蛋白质或有机化合物的位置 [75] 。硅质囊膜和SDV含量控制微形态发生,即生化硅化本身。

当在实验中将变化引入这些机制时,它们会导致形成不同的硅质结构,因此在进化过程中有些相似的变化应该创造了当前的硅藻多样性。例如,在硅藻进化早期,环带相关基因的可能突变可能是硅藻类分离的原因,因为环带结构决定了瓣膜的形状和对称性。另一方面,调节细胞骨架和囊泡运输的蛋白质突变可能会导致瓣膜更精细的模式发生变化。

因此,硅藻形态发生背后的细胞机制大多已确定,但仍有必要检测控制硅藻中物种特异性形态发生的分子遗传机制。

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