Diatoms are unicellular algae with morphologically diverse silica cell walls, which are called frustules. The mechanism of frustule morphogenesis has attracted attention in biology and nanomaterials engineering. However, the genetic regulation of the morphology remains unclear. We therefore used transcriptome sequencing to search for genes involved in frustule morphology in the centric diatom Pleurosira laevis, which exhibits morphological plasticity between flat and domed valve faces in salinity 2 and 7, respectively. We observed differential expression of transposable elements (TEs) and transporters, likely due to osmotic response. Up-regulation of mechanosensitive ion channels and down-regulation of Ca²⁺-ATPases in cells with flat valves suggested that cytosolic Ca²⁺ levels were changed between the morphologies. Calcium signaling could be a mechanism for detecting osmotic pressure changes and triggering morphological shifts. We also observed an up-regulation of ARPC1 and annexin, involved in the regulation of actin filament dynamics known to affect frustule morphology, as well as the up-regulation of genes encoding frustule-related proteins such as BacSETs and frustulin. Taken together, we propose a model in which salinity-induced morphogenetic changes are driven by upstream responses, such as the regulation of cytosolic Ca²⁺ levels, and downstream responses, such as Ca²⁺-dependent regulation of actin dynamics and frustule-related proteins. This study highlights the sensitivity of euryhaline diatoms to environmental salinity and the role of active cellular processes in controlling gross valve morphology under different osmotic pressures.

中文翻译：

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对盐度诱导的广盐硅藻 Pleurosira laevis 细胞壁形态变化的转录反应

硅藻是单细胞藻类，具有形态多样的二氧化硅细胞壁，称为硅藻壳。硅藻壳形态发生的机制引起了生物学和纳米材料工程的关注。然而，形态的遗传调控仍不清楚。因此，我们使用转录组测序来寻找与中心硅藻Pleurosira laevis中的硅藻壳形态相关的基因，该硅藻分别在盐度为2和7时表现出平坦和圆顶瓣膜面之间的形态可塑性。我们观察到转座元件（TE）和转运蛋白的差异表达，可能是由于渗透反应所致。具有扁平瓣膜的细胞中机械敏感离子通道的上调和Ca ²⁺ -ATP酶的下调表明细胞质Ca ²⁺水平在不同形态之间发生了变化。钙信号传导可能是检测渗透压变化和触发形态变化的机制。我们还观察到 ARPC1 和膜联蛋白的上调，参与已知影响硅藻壳形态的肌动蛋白丝动力学的调节，以及编码硅藻壳相关蛋白（如 BacSET 和 frustulin）的基因的上调。综上所述，我们提出了一个模型，其中盐度诱导的形态发生变化是由上游反应（例如胞质 Ca ²⁺水平的调节）和下游反应（例如肌动蛋白动力学和硅藻相关的Ca ²⁺依赖性调节）驱动的蛋白质。这项研究强调了广盐硅藻对环境盐度的敏感性以及活跃细胞过程在不同渗透压下控制总瓣膜形态中的作用。