Graduate School of Biostudies, Kyoto University, Kyoto, Japan.
RIKEN Center for Sustainable Resource Science, Kanagawa, 230-0045 Japan.
Plant Cell Physiol. 2019 Apr 1;60(4):916-930. doi: 10.1093/pcp/pcz010.
Nutrient-deprived microalgae accumulate triacylglycerol (TAG) in lipid droplets. A dual-specificity tyrosine phosphorylation-regulated kinase, TAG accumulation regulator 1 (TAR1) has been shown to be required for acetate-dependent TAG accumulation and the degradation of chlorophyll and photosynthesis-related proteins in photomixotrophic nitrogen (N)-deficient conditions (Kajikawa et�al. 2015). However, this previous report only examined particular condition. Here, we report that in photoautotrophic N-deficient conditions, tar1-1 cells, with a mutation in the TAR1 gene, maintained higher levels of cell viability and lower levels of hydrogen peroxide generation and accumulated higher levels of TAG and starch compared with those of wild type (WT) cells with bubbling of air containing 5% carbon dioxide. Transcriptomic analyses suggested that genes involved in the scavenging of reactive oxygen species are not repressed in tar1-1 cells. In contrast, the mating efficiency and mRNA levels of key regulatory genes for gametogenesis, MID, MTD and FUS, were suppressed in tar1-1 cells. Among the TAR1-dependent phosphopeptides deduced by phosphoproteomic analysis, protein kinases and enzymes related to N assimilation and carbon (C) metabolism are of particular interest. Characterization of these putative downstream factors may elucidate the molecular pathway whereby TAR1 mediates cellular propagation and C and N metabolism in C/N-imbalanced stress conditions.
营养缺乏的微藻在脂滴中积累三酰基甘油(TAG)。已经表明,双特异性酪氨酸磷酸化调节激酶 TAG 积累调节因子 1(TAR1)对于依赖于乙酸盐的 TAG 积累以及在光混合营养氮(N)缺乏条件下叶绿素和光合作用相关蛋白的降解是必需的(Kajikawa 等人,2015 年)。然而,之前的报告仅检查了特定条件。在这里,我们报告在光自养 N 缺乏条件下,具有 TAR1 基因突变的 tar1-1 细胞保持更高的细胞活力水平,更低的过氧化氢生成水平,并积累更高水平的 TAG 和淀粉与含有 5%二氧化碳的空气鼓泡的野生型(WT)细胞相比。转录组学分析表明,参与活性氧清除的基因在 tar1-1 细胞中没有被抑制。相比之下,在 tar1-1 细胞中,配子发生的关键调节基因 MID、MTD 和 FUS 的交配效率和 mRNA 水平受到抑制。在磷酸化蛋白质组学分析推断的 TAR1 依赖性磷酸肽中,与氮同化和碳(C)代谢相关的蛋白激酶和酶特别有趣。这些假定的下游因子的特征可能阐明 TAR1 在 C/N 失衡应激条件下介导细胞增殖和 C 和 N 代谢的分子途径。