Institute of Plant Biology, Biological Research Centre, Hungarian Academy of Sciences, Szeged, Hungary.
Institute of Materials and Environmental Chemistry, Research Centre for Natural Sciences Hungarian Academy of Sciences, Budapest, Hungary.
Plant J. 2018 May;94(3):548-561. doi: 10.1111/tpj.13878. Epub 2018 Mar 31.
Sulphur limitation may restrain cell growth and viability. In the green alga Chlamydomonas reinhardtii, sulphur limitation may induce H production lasting for several days, which can be exploited as a renewable energy source. Sulphur limitation causes a large number of physiological changes, including the inactivation of photosystem II (PSII), leading to the establishment of hypoxia, essential for the increase in hydrogenase expression and activity. The inactivation of PSII has long been assumed to be caused by the sulphur-limited turnover of its reaction center protein PsbA. Here we reinvestigated this issue in detail and show that: (i) upon transferring Chlamydomonas cells to sulphur-free media, the cellular sulphur content decreases only by about 25%; (ii) as demonstrated by lincomycin treatments, PsbA has a significant turnover, and other photosynthetic subunits, namely RbcL and CP43, are degraded more rapidly than PsbA. On the other hand, sulphur limitation imposes oxidative stress early on, most probably involving the formation of singlet oxygen in PSII, which leads to an increase in the expression of GDP-L-galactose phosphorylase, playing an essential role in ascorbate biosynthesis. When accumulated to the millimolar concentration range, ascorbate may inactivate the oxygen-evolving complex and provide electrons to PSII, albeit at a low rate. In the absence of a functional donor side and sufficient electron transport, PSII reaction centers are inactivated and degraded. We therefore demonstrate that the inactivation of PSII is a complex and multistep process, which may serve to mitigate the damaging effects of sulphur limitation.
硫限制可能会抑制细胞生长和活力。在绿藻莱茵衣藻中，硫限制可能会诱导持续数天的 H 生成，这可以作为一种可再生能源加以利用。硫限制会引起大量生理变化，包括破坏光合系统 II（PSII），导致缺氧建立，这对于增加氢化酶的表达和活性至关重要。PSII 的失活长期以来一直被认为是由其反应中心蛋白 PsbA 的硫限制周转引起的。在这里，我们详细重新研究了这个问题，并表明：（i）将衣藻细胞转移到无硫培养基中时，细胞中的硫含量仅减少约 25%；（ii）如林可霉素处理所示，PsbA 有明显的周转，其他光合亚基，即 RbcL 和 CP43，比 PsbA 降解得更快。另一方面，硫限制很早就会造成氧化应激，很可能涉及 PSII 中单线态氧的形成，这导致 GDP-L-半乳糖磷酸化酶的表达增加，在抗坏血酸生物合成中发挥重要作用。当积累到毫摩尔浓度范围时，抗坏血酸可能会使放氧复合酶失活，并向 PSII 提供电子，尽管速率较低。在没有功能供体侧和足够的电子传递的情况下，PSII 反应中心失活并降解。因此，我们证明 PSII 的失活是一个复杂的多步骤过程，可能有助于减轻硫限制的破坏作用。
