THE TEMPERATURE-DEPENDENCE OF THE REDOX STATE OF Q(A) AND SUSCEPTIBILITY OF PHOTOSYNTHESIS TO PHOTOINHIBITION

Citation
G. Oquist et al., THE TEMPERATURE-DEPENDENCE OF THE REDOX STATE OF Q(A) AND SUSCEPTIBILITY OF PHOTOSYNTHESIS TO PHOTOINHIBITION, Plant physiology and biochemistry, 31(5), 1993, pp. 683-691
Citations number
48
Categorie Soggetti
Plant Sciences
ISSN journal
09819428
Volume
31
Issue
5
Year of publication
1993
Pages
683 - 691
Database
ISI
SICI code
0981-9428(1993)31:5<683:TTOTRS>2.0.ZU;2-V
Abstract
The relationship between the redox state of primary, stable quinone ac ceptor of photosystem II (Q(A)) and the susceptibility of photosynthes is to photoinhibition at different temperatures was investigated. Non- hardened and cold-hardened seedlings of winter rye, and of winter and spring cultivars of wheat, were obtained by growth at either 20/16-deg rees-C (day/night) or 5/5-degrees-C (day/night), respectively. A singl e, curvi-linear relationship was established between the steady-state redox level Of Q(A) and the susceptibility of photosynthesis to short- term (8 h) photoinhibition at 5 or 25-degrees-C when spring and winter cultivars of rye and wheat, in non-hardened or cold-hardened states, were plotted together. Furthermore, irrespective of temperature (0 to 25-degrees-C) or state of cold-hardiness, the susceptibility of photos ynthesis to photoinhibition was controlled fully in winter rye by the redox state Of Q(A); e.g. similar susceptibilities to photoinhibition were obtained at 0, 5 and 25-degrees-C provided that the photon fluenc e rate at the different temperatures was adjusted to keep 50% of the p hotosystem II reaction centres in a closed state under steady-state il lumination. Our results suggest that the primary reason plants become prone to photoinhibition at low temperatures is that the proportion of closed reaction centres increases due to the low temperature imposed constraints on photosynthesis. Thus, we propose that low temperature s ensitized photoinhibition results from low temperature inhibition of p hotosynthesis rather than from low temperature inhibition of the photo system II repair cycle.