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Expression of the isiA gene is essential for the survival of the cyanobacterium Synechococcus sp. PCC 7942 by protecting photosystem II from excess light under iron limitation
Author(s) -
Park YounIl,
Sandström Stefan,
Gustafsson Petter,
Öquist Gunnar
Publication year - 1999
Publication title -
molecular microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.857
H-Index - 247
eISSN - 1365-2958
pISSN - 0950-382X
DOI - 10.1046/j.1365-2958.1999.01332.x
Subject(s) - biology , photoinhibition , photosystem ii , photosynthesis , photosystem i , synechococcus , cyanobacteria , wild type , chlorophyll , botany , biophysics , photoprotection , biochemistry , gene , mutant , genetics , bacteria
Iron deficiency is known to suppress primary productivity in both marine and freshwater ecosystems. In response to iron deficiency, certain cyanobacteria induce a chlorophyll (Chl)–protein complex, CP43′, which is encoded by the isiA gene. The deduced amino‐acid sequence of CP43′ predicts some structural similarity to the CP43 polypeptide of photosystem II, but the function of CP43′ remains uncertain. In order to assess its physiological role, the isiA gene of a cyanobacterium, Synechococcus sp. PCC7942, was inactivated by insertion mutagenesis (giving isiA − cells). Compared with isiA − cells, under iron deprivation, wild‐type cells showed both lower rates of photosystem II‐mediated O 2 evolution at limiting light irradiances and decreased yields of room temperature Chl fluorescence at various irradiances. These observations strongly suggest that the decreased photosystem II activity in wild‐type cells with CP43′ is attributable to increased non‐radiative dissipation of light energy. In agreement with this hypothesis, isiA − cells were more susceptible to photoinhibition of photosynthesis than wild‐type cells, resulting in much slower growth rates under iron limitation. Based on these results, we suggest that CP43′ functions as a non‐radiative dissipator of light energy, thus protecting photosystem II from excessive excitation under iron‐deficient conditions.