Institute of Basic Biological Problems, Russian Academy of Sciences, Institutskaya Street 2, Pushchino, Moscow Region 142290, Russia.
Institute of Basic Biological Problems, Russian Academy of Sciences, Institutskaya Street 2, Pushchino, Moscow Region 142290, Russia.
Biochim Biophys Acta Bioenerg. 2018 Apr;1859(4):292-299. doi: 10.1016/j.bbabio.2018.01.009. Epub 2018 Feb 2.
It is known, that the multi-subunit complex of photosystem II (PSII) and some of its single proteins exhibit carbonic anhydrase activity. Previously, we have shown that PSII depletion of HCO/CO as well as the suppression of carbonic anhydrase activity of PSII by a known inhibitor of α‑carbonic anhydrases, acetazolamide (AZM), was accompanied by a decrease of electron transport rate on the PSII donor side. It was concluded that carbonic anhydrase activity was required for maximum photosynthetic activity of PSII but it was not excluded that AZM may have two independent mechanisms of action on PSII: specific and nonspecific. To investigate directly the specific influence of carbonic anhydrase inhibition on the photosynthetic activity in PSII we used another known inhibitor of α‑carbonic anhydrase, trifluoromethanesulfonamide (TFMSA), which molecular structure and physicochemical properties are quite different from those of AZM. In this work, we show for the first time that TFMSA inhibits PSII carbonic anhydrase activity and decreases rates of both the photo-induced changes of chlorophyll fluorescence yield and the photosynthetic oxygen evolution. The inhibitory effect of TFMSA on PSII photosynthetic activity was revealed only in the medium depleted of HCO/CO. Addition of exogenous HCO or PSII electron donors led to disappearance of the TFMSA inhibitory effect on the electron transport in PSII, indicating that TFMSA inhibition site was located on the PSII donor side. These results show the specificity of TFMSA action on carbonic anhydrase and photosynthetic activities of PSII. In this work, we discuss the necessity of carbonic anhydrase activity for the maximum effectiveness of electron transport on the donor side of PSII.
众所周知，光系统 II（PSII）的多亚基复合物及其某些单体蛋白具有碳酸酐酶活性。先前，我们已经表明，PSII 中 HCO/CO 的耗竭以及已知的α-碳酸酐酶抑制剂乙酰唑胺（AZM）对 PSII 碳酸酐酶活性的抑制作用，伴随着 PSII 供体侧电子传递速率的降低。结论是碳酸酐酶活性是 PSII 最大光合作用所必需的，但不能排除 AZM 可能对 PSII 具有两种独立的作用机制：特异性和非特异性。为了直接研究碳酸酐酶抑制对 PSII 光合作用的特异性影响，我们使用了另一种已知的α-碳酸酐酶抑制剂三氟甲磺酸（TFMSA），其分子结构和物理化学性质与 AZM 有很大的不同。在这项工作中，我们首次表明 TFMSA 抑制 PSII 碳酸酐酶活性，并降低光诱导叶绿素荧光产额变化和光合氧气释放的速率。只有在 HCO/CO 耗尽的培养基中，TFMSA 才会抑制 PSII 的光合作用活性。添加外源性 HCO 或 PSII 电子供体导致 TFMSA 对 PSII 电子传递的抑制作用消失，表明 TFMSA 的抑制位点位于 PSII 的供体侧。这些结果表明 TFMSA 对碳酸酐酶和 PSII 光合作用活性的作用具有特异性。在这项工作中，我们讨论了碳酸酐酶活性对于 PSII 供体侧电子传递最大效率的必要性。
