EXPRESSION OF THE PSBA GENE DURING PHOTOINHIBITION AND RECOVERY IN SYNECHOCYSTIS PCC-6714 - INHIBITION AND DAMAGE OF TRANSCRIPTIONAL AND TRANSLATIONAL MACHINERY PREVENT THE RESTORATION OF PHOTOSYSTEM-II ACTIVITY
S. Constant et al., EXPRESSION OF THE PSBA GENE DURING PHOTOINHIBITION AND RECOVERY IN SYNECHOCYSTIS PCC-6714 - INHIBITION AND DAMAGE OF TRANSCRIPTIONAL AND TRANSLATIONAL MACHINERY PREVENT THE RESTORATION OF PHOTOSYSTEM-II ACTIVITY, Plant molecular biology, 34(1), 1997, pp. 1-13
The D1 reaction center protein of the photosystem II complex is very s
ensitive to light. It is continuously being damaged, degraded and resy
nthesized. Under high light, photosystem II inactivation is observed.
This is because the rate of D1 damage is faster than that of its repla
cement. This process can be reversed if exposure to high light is not
too long. In this work we study the changes that occur in the transcri
ptional and translational machinery that could lead to irreversible ph
otoinhibition in Synechocystis PCC 6714. In the first minutes of photo
inhibition, high light induced an accumulation of psbA mRNA due to an
increase in psbA transcription initiation. Although the transcription
rate of other photosynthetic genes (e.g. psaE and cpcB-cpcA) declined,
the high turnover of the psbA transcript was maintained for a long ti
me. When the light stress was too long, the stability of psbA mRNA inc
reased and the psbA transcription rate appeared to decrease. A high le
vel of psbA mRNA was maintained even though translation no longer occu
rred and the cells were unable to recover. Experiments to measure newl
y synthesized D1 incorporation into the thylakoid membranes during rec
overy in the presence of rifampicin showed that the initiation of tran
scription was not required for translation of psbA mRNA when photoinhi
bition was still reversible. Since psbA translation did not depend on
the level of psbA transcript or on the initiation of psbA transcriptio
n, we propose that damage to the translational machinery also occurred
during light stress, leading to the inhibition of D1 synthesis and to
irreversible photoinhibition.