The effect of Photosystem II inhibitors DCMU and BNT on the high-light induced D1 turnover in two cyanobacterial strains Synechocystis PCC 6803 and Synechococcus PCC 7942

The effect of the Photosystem II (PSII) inhibitors dichlorophenyldimethylurea (DCMU) and bromonitrothymol (BNT) on the rate of the high-light induced D1 protein turnover was studied in whole cells of two cyanobacterial strains Synechocystis PCC 6803 and Synechococcus PCC 7942. In Synechocystis the D1 degradation was slowed down to a similar extent in the presence of either inhibitor compared with control cells. This slower degradation corresponded with the retardation of Photosystem II photoinactivation (PSIIPI) measured as a decline of PS II activity in the illuminated cells treated with chloramphenicol (CAP). The ongoing DI synthesis in the presence of both PS II inhibitors was confirmed by unchanging PS II activity and the steady-state level of D1 during illumination in the absence of CAP. In Synechococcus cells both DCMU and BNT blocked the turnover of the 'low-light' D1 form (D1:1) but did not prevent the exchange of the 'high-light' form D1:2 for the D1:1 form. The similar effect of both herbicides on the D1 exchange was in contrast with their influence on the rate of PSIIPI. While DCMU had a pronounced protective effect, BNT significantly increased the rate of PS II photodamage. The fast BNT-induced decline of PS II activity was also observed in Synechocystis cells treated with azide, an inhibitor of reactive oxygen species scavenging enzymes. Therefore, we assume that the distinct sensitivity of the two cyanobacterial strains to BNT can be caused by different content and/or activity of these enzymes in each strain.