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MV inhibited growth, light-saturated 0 2 evolution, and PS II activity
(tested by delayed light emission) in the PCC 7942
sodB
.mutant within
8 hr of stress treatment. In contrast, the PCC 7942 wild type remained
nearly unaffected for 48 hr of 0.5 pM MV treatment. The oxidative
damage to photosynthesis of the PCC 7942
sodB'
mutant was not
accompanied by essential changes in chlorophyll content and
carotene/chlorophyll ratio (Table I) but was accompanied by greater
catalase activity (Table 2).
Table 1. Chlorophyll content and carotene/chlorophyll ratio (measured
in acetone extracts [6]) in the
Synechococcus
sp. PCC 7942 wild type
and
sodB'
mutant cultures started at normal growth conditions and then
exposed to 0.5 pM IV
V at the same growth conditions.
Synecho
coccus
sp. PCC
7942
Time of
growth,
hr
Chlorophyll, pg ■lO-6
cells (means ± SD)
Carotene/ch lorophy1
(means
±
SD)
Control
With 0.5
pM MV
Control
With 0.5
pM MV
Wild
type
6
0.163 +
0.027
0.167 ±
0.001
5.75 +
0.13
5.76 ±
0.06
24
0.161 ±
0.011
0.155 ±
0.003
5.97 ±
0.38
5.87 ±
0.31
48
0.151 ±
0.003
0.166 ±
0.002
5.92 +
0.36
5.90 +
0.11
SodB'
mutant
6
0.136 ±
0.012
0.121 ±
0.027
6.26 +
0.44
6.12 ±
0.25
24
0.130 ±
0.019
0.098 ±
0.011
5.84 +
0.69
5.78 ±
0.39
48
0.131 ±
0.009
0.105 ±
0.021
5.74 +
0.19
5.67 +
0.23
Earlier [5], it was demonstrated in the PCC 7942
sodB'
mutant
that PS II activity, PS I cyclic activity, and the P700 reaction center are
all targets of CV formed at PS I and that the cytosolic superoxide
dismutase (Fe-SOD) protects these targets from oxidative damage. The
earliest of these targets to be damaged by MV in the absence of
sodB
gene is PS I cyclic electron transport. This observation is consistent
with the vulnerability of Fe4S
4
clusters of PS I to disruption by
414
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