COMPROMISED HYDROLYSIS OF TRIACYLGLYCEROLS7 (CHT7) in Chlamydomonas (Chlamydomonas reinhardtii) was previously shown to affect the transcription of a subset of genes during nitrogen (N)-replete growth and following N refeeding. Here, we show that an extensive derepression of genes involved in DNA metabolism and cell cycle–related processes, as well as downregulation of genes encoding oxidoreductases and nutrient transporters, occurs in the cht7 mutant during N deprivation. Cellular mutant phenotypes are consistent with the observed transcriptome misregulation, as cht7 cells fail to properly arrest growth, nuclear replication, and cell division following N deprivation. Reduction in cht7 colony formation following N refeeding is explained by its compromised viability during N deprivation and by the occurrence of abortive divisions during N refeeding. Surprisingly, the largely unstructured C-terminal half of CHT7 with predicted protein binding domains, but not the canonical CXC DNA binding domain, is essential for the ability of CHT7 to form stable complexes and reverse the cellular phenotypes and transcription levels in the cht7 mutant. Hence, although lacking the presumed DNA binding domain, CHT7 modulates the expression of cell cycle genes in response to N availability, which is essential for establishing an effective quiescent state and the coordinated resumption of growth following N refeeding.

先前显示，衣藻（Chlamydomonas reinhardtii）的透化的三酰甘油7（CHT7）水解会影响全氮（N）生长和N补饲后基因子集的转录。在这里，我们表明在N剥夺过程中，cht7突变体会广泛抑制涉及DNA代谢和细胞周期相关过程的基因，以及编码氧化还原酶和营养转运蛋白的基因的下调。细胞突变表型与观察到的转录组调控异常一致，因为cht7细胞不能在N剥夺后适当阻止生长，核复制和细胞分裂。减少cht7补氮后菌落形成的原因是其在剥夺氮的过程中丧失了生存能力，以及补氮时发生了分裂性分裂。出乎意料的是，CHT7的大部分非结构化的C末端一半具有预测的蛋白结合结构域，而不是规范的CXC DNA结合结构域，对于CHT7形成稳定复合物并逆转cht7突变体中细胞表型和转录水平的能力至关重要。因此，尽管缺乏推测的DNA结合结构域，但是CHT7响应N的可利用性而调节细胞周期基因的表达，这对于建立有效的静止状态和N补充后的协调生长恢复是必不可少的。