Laboratory of Bioenergetics, Institute of Plant Biology B22, University of Liège, Belgium.
J Biotechnol. 2012 Nov 30;162(1):81-8. doi: 10.1016/j.jbiotec.2012.07.002. Epub 2012 Jul 24.
The relative contributions of the PSII-dependent and Nda2-dependent pathways for H₂ photoproduction were investigated in the green microalga Chlamydomonas reinhardtii after suphur-deprivation. For this purpose, H₂ gas production was compared for wild-type and Nda2-deficient cells with or without DCMU (a PSII-inhibitor) in the same experimental conditions. Nda2-deficiency caused a 30% decrease of the maximal H₂ photoevolution rate observed shortly after the establishment of anoxia, and an acceleration of the decline of H₂ photoevolution rate with time. DCMU addition to Nda2-deficient cells completely inhibited H₂ photoproduction, showing that the PSII-independent H₂ photoproduction relies on the presence of Nda2, which feeds the photosynthetic electron transport chain with electrons derived from oxidative catabolism. Nda2-protein abundance increased as a result of sulphur deprivation and further during the H₂ photoproduction process, resulting in high rates of non-photochemical plastoquinone reduction in control cells. Nda2-deficiency had no significant effect on photosynthetic and respiratory capacities in sulphur-deprived cells, but caused changes in the cell energetic status (ATP and NADPH/NADP+ ratio). The rapid decline of H₂ photoevolution rate with time in Nda2-deficient cells revealed a more pronounced inhibition of H₂ photoproduction by accumulated H₂ in the absence of non-photochemical plastoquinone reduction. Nda2 is therefore important for linking H₂ photoproduction with catabolism of storage carbon compounds, and seems also involved in regulating the redox poise of the photosynthetic electron transport chain during H₂ photoproduction.
在硫饥饿后,研究了 PSII 依赖性和 Nda2 依赖性途径对莱茵衣藻中 H₂光生产的相对贡献。为此,在相同的实验条件下,比较了野生型和 Nda2 缺陷细胞在有或没有 DCMU(PSII 抑制剂)的情况下的 H₂气体产生。Nda2 缺陷导致缺氧建立后不久观察到的最大 H₂光进化率降低了 30%,并且随着时间的推移 H₂光进化率的下降加速。DCMU 添加到 Nda2 缺陷细胞中完全抑制了 H₂光生产,表明 PSII 非依赖性 H₂光生产依赖于 Nda2 的存在,Nda2 从氧化分解代谢中为光合作用电子传递链提供电子。硫饥饿导致 Nda2 蛋白丰度增加,并且在 H₂光生产过程中进一步增加,导致对照细胞中质体醌的非光化学还原率很高。Nda2 缺陷对硫饥饿细胞中的光合和呼吸能力没有显著影响,但导致细胞能量状态(ATP 和 NADPH/NADP+ 比)发生变化。在 Nda2 缺陷细胞中,H₂光进化率随时间的快速下降表明,在没有非光化学质体醌还原的情况下,积累的 H₂对 H₂光生产的抑制作用更为明显。因此,Nda2 对于将 H₂光生产与储存碳化合物的分解代谢联系起来很重要,并且似乎也参与了在 H₂光生产过程中调节光合作用电子传递链的氧化还原平衡。