Inactivation of the extrinsic subunit of photosystem II, PsbU, in Synechococcus PCC 7942 results in elevated resistance to oxidative stress

Abstract

PsbU is a subunit of the extrinsic complex attached to the core of photosystem II. A PsbU-mutant of Synechococcus PCC 7942 was isolated based on its elevated resistance to externally applied oxidative stress. PsbU-mutant exhibits fast rates of degradation of the photosystem II core protein, D1, under subsaturating as well as high-light conditions. While forward electron transfer is not affected, back electron flow is severely impaired in the mutant. We suggest that impairment of psbU results in production of reactive-oxygen-species, which trigger antioxidative mechanisms even under standard growth conditions. Accordingly, when challenged with external oxidative stress, these cells are more resistant than wild type cells.

The role of the orange carotenoid protein and PsbU protein in photoprotection in cyanobacteria

“…In the presence of DCMU, the main fluorescence decay component, which reflects the recombination of Q A -with the S 2 state is slower in the mutant (T 3 ~3.4 s) than in the wild type (T 3 ~1.6 s) , which is in agreement with previous data (Balint et al, 2006) (Fig.4.10.B, Table 1). …”

“…In a study by Balint et al it was reported that the rate of the forward electron transport from Q A -to Q B was not affected by the absence of the PsbU subunit, while the S 2 Q A -charge recombination process is slowed down in Synechococcus 7942 (Balint et al, 2006). However, flash fluorescence data presented in that study were rather noisy, and the different phases of the fluorescence decay could not be clearly resolved.…”

“…It has been reported that removal of PsbU altered primary photochemical processes and led to the accumulation of uncoupled phycobilisomes decreasing the energy transfer from PBs to PSII (Veerman et al, 2005). Recently, flash-induced Chl fluorescence decay and thermoluminescence (TL) measurements performed with a PsbU mutant of Synechococcus PCC 7942 showed that the rate of charge recombination from the S 2 Q A -state is slowed down, as shown by the retarded rate of fluorescence decay and the upshifted peak position of the Q band in the presence of the electron transport inhibitor DCMU (Balint et al, 2006). Balint et al also proposed that PsbU provides protection from reactive oxygen species because PsbU mutants have exhibited higher resistance to oxidative stress compared with the wild type strain.…”

“…The PsbU protein stabilizes the PSII complex in several ways. The absence of PsbU results 352 2 in the reduction of the rate of oxygen evolution (Shen et al, 1997;Inoue-Kashino et al, 2005) and a high sensitivity of cells to photodamage, resulting in rapid degradation of the D1 protein (Inoue-Kashino et al, 2005;Balint et al, 2006 (Shen et al, 1997). Shen et al (1997) demonstrated that the peak temperatures of both the thermoluminescence Q and B bands were increased by 4 o C in ∆PsbU Synechocystis mutant cells compared to wild type cells.…”

“…However, Synechococcus cells were sensitive to freezing, which led to the loss of TL signal intensity (not shown), and made it even undetectable in the ∆PsbU mutant in the absence of DCMU (Balint et al, 2006). In order to avoid this freezing effect, the standard protocol was changed and TL curves were recorded from 0 to 80 °C (with a saturating flash at +5 °C) in the absence of DCMU, and from -4 to 80 °C (with saturating flash at -2 °C) in the presence of DCMU.…”