Oxygen-dependent electron flow influences photosystem II function and psbA gene expression in the cyanobacterium Synechococcus sp. PCC 7942. Campbell, D., Clarke, A. K., Gustafsson, P., & Öquist, G. Physiologia Plantarum, 105(4):746–755, 1999. _eprint: https://onlinelibrary.wiley.com/doi/pdf/10.1034/j.1399-3054.1999.105420.x![Oxygen-dependent electron flow influences photosystem II function and psbA gene expression in the cyanobacterium Synechococcus sp. PCC 7942 [link]](https://bibbase.org/img/filetypes/link.svg "link")
Paper doi abstract bibtex During acclimated growth in Synechococcus sp. PCC 7942 a substantial proportion of the electrons extracted from water by photosystem II ultimately flow back to oxygen. This flow increases rapidly under high light, which allows Synechococcus to maintain photosystem II centers largely open, even under excessive excitation. The electron flow to oxygen with increasing light accounts for the progressive discrepancy between the light response curve of measured oxygen evolution, and the light response curve of photosystem II activity estimated from fluorescence measures. In cells under anoxia this flexible electron sink is lost and photosystem II centers suffer partial closure at the growth light intensity, with closure becoming more severe under excess light. As predicted from earlier work this PSII closure results in rapid loss of psbAI message, encoding the D1:1 protein of PSII, and induction of psbAII/AIII encoding the alternate D1:2 protein. The changes in the mRNA pool are not, however, reflected at the protein level, and D1:1 remains in the thylakoid membranes. There is no accumulation of D1:2, despite some continued synthesis of other proteins. PSII closure, therefore, results in repression of psbAI and induction psbAII/AIII expression, but D1:1/D1:2 exchange is blocked by anoxia, downstream from transcription. D1:1 protein and PSII activity are quite stable under anoxia and moderate illumination. Nevertheless, upon recovery under oxygenic conditions, the existing D1:1 is lost from the membranes, resulting in a transient drop in PSII activity. This suggests that under normal conditions the cells use oxygen to facilitate preemptive turnover of D1 proteins.
@article{campbell_oxygen-dependent_1999,
title = {Oxygen-dependent electron flow influences photosystem {II} function and {psbA} gene expression in the cyanobacterium {Synechococcus} sp. {PCC} 7942},
volume = {105},
issn = {1399-3054},
url = {https://onlinelibrary.wiley.com/doi/abs/10.1034/j.1399-3054.1999.105420.x},
doi = {10.1034/j.1399-3054.1999.105420.x},
abstract = {During acclimated growth in Synechococcus sp. PCC 7942 a substantial proportion of the electrons extracted from water by photosystem II ultimately flow back to oxygen. This flow increases rapidly under high light, which allows Synechococcus to maintain photosystem II centers largely open, even under excessive excitation. The electron flow to oxygen with increasing light accounts for the progressive discrepancy between the light response curve of measured oxygen evolution, and the light response curve of photosystem II activity estimated from fluorescence measures. In cells under anoxia this flexible electron sink is lost and photosystem II centers suffer partial closure at the growth light intensity, with closure becoming more severe under excess light. As predicted from earlier work this PSII closure results in rapid loss of psbAI message, encoding the D1:1 protein of PSII, and induction of psbAII/AIII encoding the alternate D1:2 protein. The changes in the mRNA pool are not, however, reflected at the protein level, and D1:1 remains in the thylakoid membranes. There is no accumulation of D1:2, despite some continued synthesis of other proteins. PSII closure, therefore, results in repression of psbAI and induction psbAII/AIII expression, but D1:1/D1:2 exchange is blocked by anoxia, downstream from transcription. D1:1 protein and PSII activity are quite stable under anoxia and moderate illumination. Nevertheless, upon recovery under oxygenic conditions, the existing D1:1 is lost from the membranes, resulting in a transient drop in PSII activity. This suggests that under normal conditions the cells use oxygen to facilitate preemptive turnover of D1 proteins.},
language = {en},
number = {4},
urldate = {2021-11-08},
journal = {Physiologia Plantarum},
author = {Campbell, Douglas and Clarke, Adrian K. and Gustafsson, Petter and Öquist, Gunnar},
year = {1999},
note = {\_eprint: https://onlinelibrary.wiley.com/doi/pdf/10.1034/j.1399-3054.1999.105420.x},
pages = {746--755},
}
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The electron flow to oxygen with increasing light accounts for the progressive discrepancy between the light response curve of measured oxygen evolution, and the light response curve of photosystem II activity estimated from fluorescence measures. In cells under anoxia this flexible electron sink is lost and photosystem II centers suffer partial closure at the growth light intensity, with closure becoming more severe under excess light. As predicted from earlier work this PSII closure results in rapid loss of psbAI message, encoding the D1:1 protein of PSII, and induction of psbAII/AIII encoding the alternate D1:2 protein. The changes in the mRNA pool are not, however, reflected at the protein level, and D1:1 remains in the thylakoid membranes. There is no accumulation of D1:2, despite some continued synthesis of other proteins. PSII closure, therefore, results in repression of psbAI and induction psbAII/AIII expression, but D1:1/D1:2 exchange is blocked by anoxia, downstream from transcription. D1:1 protein and PSII activity are quite stable under anoxia and moderate illumination. Nevertheless, upon recovery under oxygenic conditions, the existing D1:1 is lost from the membranes, resulting in a transient drop in PSII activity. This suggests that under normal conditions the cells use oxygen to facilitate preemptive turnover of D1 proteins.","language":"en","number":"4","urldate":"2021-11-08","journal":"Physiologia Plantarum","author":[{"propositions":[],"lastnames":["Campbell"],"firstnames":["Douglas"],"suffixes":[]},{"propositions":[],"lastnames":["Clarke"],"firstnames":["Adrian","K."],"suffixes":[]},{"propositions":[],"lastnames":["Gustafsson"],"firstnames":["Petter"],"suffixes":[]},{"propositions":[],"lastnames":["Öquist"],"firstnames":["Gunnar"],"suffixes":[]}],"year":"1999","note":"_eprint: https://onlinelibrary.wiley.com/doi/pdf/10.1034/j.1399-3054.1999.105420.x","pages":"746–755","bibtex":"@article{campbell_oxygen-dependent_1999,\n\ttitle = {Oxygen-dependent electron flow influences photosystem {II} function and {psbA} gene expression in the cyanobacterium {Synechococcus} sp. {PCC} 7942},\n\tvolume = {105},\n\tissn = {1399-3054},\n\turl = {https://onlinelibrary.wiley.com/doi/abs/10.1034/j.1399-3054.1999.105420.x},\n\tdoi = {10.1034/j.1399-3054.1999.105420.x},\n\tabstract = {During acclimated growth in Synechococcus sp. PCC 7942 a substantial proportion of the electrons extracted from water by photosystem II ultimately flow back to oxygen. This flow increases rapidly under high light, which allows Synechococcus to maintain photosystem II centers largely open, even under excessive excitation. The electron flow to oxygen with increasing light accounts for the progressive discrepancy between the light response curve of measured oxygen evolution, and the light response curve of photosystem II activity estimated from fluorescence measures. In cells under anoxia this flexible electron sink is lost and photosystem II centers suffer partial closure at the growth light intensity, with closure becoming more severe under excess light. As predicted from earlier work this PSII closure results in rapid loss of psbAI message, encoding the D1:1 protein of PSII, and induction of psbAII/AIII encoding the alternate D1:2 protein. 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