Department of Biological Science, Graduate School of Science, Osaka Prefecture University, 1-1 Gakuen-cho, Naka-ku, Sakai, Osaka, 599-8531 Japan.
Faculty of Liberal Arts and Sciences, Osaka Prefecture University, 1-1 Gakuen-cho, Naka-ku, Sakai, Osaka, 599-8531 Japan.
Plant Cell Physiol. 2022 Feb 15;63(2):189-199. doi: 10.1093/pcp/pcab159.
Under nitrogen (N)-limited conditions, the non-N2-fixing cyanobacterium Synechocystis sp. PCC 6803 (Synechocystis 6803) actively grows during early stages of starvation by performing photosynthesis but gradually stops the growth and eventually enters dormancy to withstand long-term N limitation. During N limitation, Synechocystis 6803 cells degrade the large light-harvesting antenna complex phycobilisomes (PBSs) presumably to avoid excess light absorption and to reallocate available N to essential functions for growth and survival. These two requirements may be driving forces for PBS degradation during N limitation, but how photosynthesis and cell growth affect PBS degradation remains unclear. To address this question, we examined involvements of photosynthesis and cell growth in PBS degradation during N limitation. Treatment of photosynthesis inhibitors and shading suppressed PBS degradation and caused non-bleaching of cells during N limitation. Limitations of photosynthesis after initial gene responses to N limitation suppressed PBS degradation, implying that photosynthesis affects PBS degradation in a post-translational manner. In addition, limitations of cell growth by inhibition of peptidoglycan and fatty acid biosynthesis, low growth temperature and phosphorous starvation suppressed PBS degradation during N limitation. Because decreased photosynthetic activity led to decreased cell growth, and vice versa, photosynthesis and cell growth would inseparably intertwine each other and affect PBS degradation during N limitation in a complex manner. Our data shed light on the coordination mechanisms among photosynthesis, cell growth and PBS degradation during N limitation.
在氮(N)限制条件下,非固氮蓝藻集胞藻 6803(Synechocystis 6803)在饥饿的早期阶段通过光合作用积极生长,但随着时间的推移逐渐停止生长,最终进入休眠状态以耐受长期的 N 限制。在 N 限制期间,Synechocystis 6803 细胞降解大型光捕获天线复合物藻胆体(PBS),这可能是为了避免过量的光吸收,并将可用的 N 重新分配到生长和存活所必需的功能上。这两个需求可能是 PBS 在 N 限制期间降解的驱动力,但光合作用和细胞生长如何影响 PBS 降解仍不清楚。为了解决这个问题,我们研究了光合作用和细胞生长在 N 限制期间 PBS 降解中的作用。光合作用抑制剂和遮光处理抑制了 PBS 的降解,并导致在 N 限制期间细胞不发生漂白。在 N 限制初始基因反应后光合作用的限制抑制了 PBS 的降解,这表明光合作用以翻译后方式影响 PBS 的降解。此外,肽聚糖和脂肪酸生物合成的抑制、低温和磷饥饿限制了细胞生长,这些都抑制了 N 限制期间 PBS 的降解。因为光合作用活性的降低会导致细胞生长的减少,反之亦然,所以在 N 限制期间,光合作用和细胞生长将以复杂的方式不可分割地交织在一起,并影响 PBS 的降解。我们的数据揭示了在 N 限制期间光合作用、细胞生长和 PBS 降解之间的协调机制。