Kobayashi Satomi, Tsuzuki Mikio, Sato Norihiro
School of Life Sciences, Tokyo University of Pharmacy and Life Sciences, Horinouchi 1432-1, Hachioji, Tokyo 192-0392, Japan.
School of Life Sciences, Tokyo University of Pharmacy and Life Sciences, Horinouchi 1432-1, Hachioji, Tokyo 192-0392, Japan JST, CREST, Chiyoda-ku, Tokyo, 102-0075, Japan.
Plant Cell Physiol. 2015 Aug;56(8):1521-32. doi: 10.1093/pcp/pcv073. Epub 2015 May 25.
Excess sulfite is well known to have toxic effects on photosynthetic activities and growth in plants, however, so far, the behavior of the photosynthetic apparatus during sulfite-stress has not been characterized as to the responsible proteins or genes. Here, the effects of sulfite on photosystem complexes were investigated in a cyanobacterium, Synechococcus elongatus PCC 7942, a possible model organism of chloroplasts. Culturing of the cells for 24 h in the presence of 10 mM sulfite retarded cell growth of the wild type, concomitantly with synthesis of Chl and phycobilisome repressed. The excess sulfite simultaneously repressed photosynthesis by more than 90%, owing largely to structural destabilization and resultant inactivation of the PSII complex, which seemed to consequently retard the cell growth. Notably, the PsbO protein, one of the subunits that construct the water-splitting system of PSII, was retained at a considerable level, and disruption of the psbO gene led to higher sensitivity of photosynthesis and growth to sulfite. Meanwhile, the PSI complex showed monomerization of its trimeric configuration with little effect on the activity. The structural alterations of these PS complexes depended on light. Our data provide evidence for quantitative decreases in the photosystem complex(es) including their antenna(e), structural alterations of the PSI and PSII complexes that would modulate their functions, and a crucial role of psbO in PSII protection, in Synechococcus cells during sulfite-stress. We suggest that the reconstruction of the photosystem complexes is beneficial to cell survival.
众所周知，过量的亚硫酸盐对植物的光合作用和生长具有毒性作用。然而，迄今为止，在亚硫酸盐胁迫期间光合装置的行为，在相关蛋白质或基因方面尚未得到表征。在此，我们以一种蓝细菌——聚球藻属的细长聚球藻PCC 7942（一种可能的叶绿体模式生物）为研究对象，探讨了亚硫酸盐对光系统复合物的影响。在10 mM亚硫酸盐存在的情况下，将细胞培养24小时会抑制野生型细胞的生长，同时叶绿素和藻胆体的合成也受到抑制。过量的亚硫酸盐同时使光合作用降低了90%以上，这主要是由于PSII复合物的结构不稳定并导致其失活，这似乎进而阻碍了细胞生长。值得注意的是，构成PSII水裂解系统的亚基之一PsbO蛋白保持在相当高的水平，并且psbO基因的破坏导致光合作用和生长对亚硫酸盐的敏感性更高。同时，PSI复合物显示其三聚体结构单体化，但对活性影响不大。这些PS复合物的结构改变取决于光照。我们的数据为亚硫酸盐胁迫期间聚球藻细胞中光系统复合物（包括其天线）的数量减少、PSI和PSII复合物的结构改变（这会调节它们的功能）以及psbO在PSII保护中的关键作用提供了证据。我们认为光系统复合物的重建有利于细胞存活。
