Scripps Institution of Oceanography, University of California, San Diego, California 92037, USA.
BMC Genomics. 2012 Sep 20;13:499. doi: 10.1186/1471-2164-13-499.
Silicon plays important biological roles, but the mechanisms of cellular responses to silicon are poorly understood. We report the first analysis of cell cycle arrest and recovery from silicon starvation in the diatom Thalassiosira pseudonana using whole genome microarrays.
Three known responses to silicon were examined, 1) silicified cell wall synthesis, 2) recovery from silicon starvation, and 3) co-regulation with silicon transporter (SIT) genes. In terms of diatom cell wall formation, thus far only cell surface proteins and proteins tightly associated with silica have been characterized. Our analysis has identified new genes potentially involved in silica formation, and other genes potentially involved in signaling, trafficking, protein degradation, glycosylation and transport, which provides a larger-scale picture of the processes involved. During silicon starvation, an overrepresentation of transcription and translation related genes were up-regulated, indicating that T. pseudonana is poised to rapidly recover from silicon starvation and resume cell cycle progression upon silicon replenishment. This is in contrast to other types of limitation, and provides the first molecular data explaining the well-established environmental response of diatoms to grow as blooms and to out-compete other classes of microalgae for growth. Comparison of our data with a previous diatom cell cycle analysis indicates that assignment of the cell cycle specific stage of particular cyclins and cyclin dependent kinases should be re-evaluated. Finally, genes co-varying in expression with the SITs enabled identification of a new class of diatom-specific proteins containing a unique domain, and a putative silicon efflux protein.
Analysis of the T. pseudonana microarray data has provided a wealth of new genes to investigate previously uncharacterized cellular phenomenon related to silicon metabolism, silicon's interaction with cellular components, and environmental responses to silicon.
硅在生物学中发挥着重要作用，但细胞对硅的反应机制仍知之甚少。我们首次利用全基因组微阵列分析了硅藻假交替单胞菌中细胞周期停滞和硅饥饿恢复的过程。
研究了三种已知的硅反应，1）硅化细胞壁合成，2）硅饥饿恢复，3）与硅转运蛋白（SIT）基因的共调控。就硅藻细胞壁的形成而言，到目前为止，只有细胞表面蛋白和与硅紧密结合的蛋白质得到了描述。我们的分析确定了新的可能参与硅形成的基因，以及其他可能参与信号转导、运输、蛋白质降解、糖基化和运输的基因，这为涉及的过程提供了更全面的描述。在硅饥饿期间，转录和翻译相关基因的上调表明，T. pseudonana 已准备好迅速从硅饥饿中恢复，并在硅补充后恢复细胞周期进程。这与其他类型的限制形成对比，并为硅藻对生长为浮游生物并与其他类型的微藻竞争生长的环境反应提供了首个分子数据解释。将我们的数据与之前的硅藻细胞周期分析进行比较表明，应该重新评估特定细胞周期蛋白和细胞周期依赖性激酶的细胞周期特定阶段的分配。最后，与 SITs 表达共变的基因能够鉴定出一类新的含有独特结构域的硅藻特异性蛋白和一种可能的硅外排蛋白。
对 T. pseudonana 微阵列数据的分析提供了丰富的新基因，可用于研究与硅代谢、硅与细胞成分相互作用以及对硅的环境反应相关的以前未被描述的细胞现象。
