Disease relevance of psaE

• A stable deletion mutation for the psaE gene was generated by transforming Synechocystis sp. PCC 6803 with a cloned DNA in which the psaE gene for 8-kDa subunit was replaced by a gene conferring resistance to kanamycin [1].

High impact information on psaE

• PCR amplification and cassette mutagenesis were used in this work to delete the psaE gene [2].
• Transferring wild-type cells from one type of illumination to another induced changes in the redox state of the electron transport chain and in psbA and psaE expression [3].
• Our data suggest that the redox state of one of the electron carriers between the plastoquinone pool and the photosystem I has opposite influences on psbA and psaE expression [3].
• In the psaE mutant, the relative petH (encoding FNR) expression level was found to be significantly increased, providing a possible explanation for the lack of a phenotype (i.e., a decrease in growth rate) that was expected from the lower rate of linear electron transport in the mutant [4].
• The process of ferredoxin reduction by photosystem I has been extensively investigated by flash-absorption spectroscopy in psaD and psaE deleted mutants from Synechocystis sp. PCC 6803 [5].

Biological context of psaE

• Subsequent analysis of psaC, psaE, psaK1, and psaLI promoters revealed that their light response was also achieved by AT-rich sequences located at the -70 to -46 region [6].

Other interactions of psaE

• Photoinhibition and light-induced cyclic electron transport in ndhB(-) and psaE(-) mutants of Synechocystis sp. PCC 6803 [7].
• 8. In the psaE deleted mutant as in the wild type, the change of pH from 8 to 5.8 induces a 10-fold increase in affinity of ferredoxin for photosystem I. In the absence of PsaD, this pH effect is not observed, in favor of this subunit being mostly responsible for the low pH increased affinity [5].

References