Marina G. Rakhimberdieva

Carotenoid-induced quenching of the phycobilisome fluorescence in photosystem II-deficient mutant of Synechocystis sp.

Brief – 10‐second long – irradiation of a photosystem II‐deficient mutant of cyanobacterium Synechocystis sp. PCC 6803 with intense blue or UV‐B light causes an about 40% decrease of phycobilisome (PBS) fluorescence, slowly reversible in the dark. The registered action spectrum of PBS fluorescence quenching only shows bands at 500, 470 and 430 nm, typical of carotenoids, and an additional UV‐B band; no peaks in the region of chlorophyll or PBS absorption have been found. We propose that quenching induced by carotenoids, possibly protein‐bound or glycoside, reveals a new regulatory mechanism protecting photosynthetic apparatus of cyanobacteria against photodamage.

Protein–protein interactions in carotenoid triggered quenching of phycobilisome fluorescence in Synechocystis sp. PCC 6803

An inquiry into the effect of temperature on carotenoid triggered quenching of phycobilisome (PBS) fluorescence in a photosystem II‐deficient mutant of Synechocystis sp. results in identification of two temperature‐dependent processes: one is responsible for the quenching rate, and one determines the yield of PBS fluorescence. Non‐Arrhenius behavior of the light‐on quenching rate suggests that carotenoid‐absorbed light triggers a process that bears a strong resemblance to soluble protein folding, showing temperature‐dependent enthalpy of activated complex formation. The response of PBS fluorescence yield to hydration changing additives and to passing of the membrane lipid phase transition point indicates that the pool size of PBSs subject to quenching depends on the state of some membrane component.

Synechocystis sp. PCC 6803 mutant lacking both photosystems exhibits strong carotenoid-induced quenching of phycobilisome fluorescence

Blue light induced quenching in a Synechocystis sp. PCC 6803 strain lacking both photosystems is only related to allophycocyanin fluorescence. A fivefold decrease in the fluorescence level in two bands near 660 and 680 nm is attributed to different allophycocyanin forms in the phycobilisome core. Some low‐heat sensitive component inactivated at 53 °C is involved in the quenching process. Enormous allophycocyanin fluorescence in the absence of the photosystems reveals a dark stage in this quenching. Thus, we present evidence that light activation of the carotenoid‐binding protein and formation of a quenching center within the phycobilisome core in vivo are discrete events in a multistep process.

Inhibition by glucose of chlorophyll a and phycocyanobilin biosynthesis in the unicellular red alga Galdieria partita at the stage of coproporphyrinogen III formation

Abstract The repression effect of d -glucose on the pigment apparatus of photosynthesis in the unicellular acidophilic red alga Galdieria partita capable of heterotrophic growth was studied. The rate of cell growth under heterotrophic conditions was higher by more than one order of magnitude than that in the autotrophic ones, and the size of those cells was larger. The addition of 1% d -glucose to the growth medium caused an increase in the number of mitochondrion profiles in the cell and a decline of thylakoid number in the chloroplast of G. partita . The loss of thylakoid membranes is accompanied by a reduction of the contents of chlorophyll a . C-phycocyanin and allophycocyanin in the heterotrophic cells. Simultaneously, switching G. partita from autotrophic growth to heterotrophic nutrition led to the excretion of coproporphyrin(ogen) III into the growth medium. Thus, the presence of d -glucose caused a reduction of pigment contents in the cell, due to the inhibition of chlorophyll a and phycocyanobilin biosynthesis at the stage of the transformation of their universal precursor, coproporphyrinogen III, to protoporphyrinogen IX. In the mixotrophic culture of G. partita light induces both the biosynthesis of photosynthetic pigments and the excretion of coproporphyrin(ogen) III. It is supposed that light affects an earlier stage in the biosynthetic pathway of chlorophyll a and phycocyanobilin than does d -glucose.

The development of carotenoid-deficient membranes in plastids of barley seedlings treated with norflurazon☆

The effect of carotenoid (Car) deficiency on the formation of thylakoid membranes in barley seedlings grown with norflurazon (NF) was investigated. To exclude photodestruction during the growth of Car-deficient seedlings, the etiolated seedlings were illuminated for 24 h with 2.5 ms flashes every 12 min. The morphometric analysis of seven main ultrastructural parameters of plastids control and NF-treated seedlings was carried out. The length of one partition and the number of partitions per plastids section, which characterize the initial stages of stacking, showed no difference in etiolated NF-treated and control seedlings. Compared with the control, the number of partitions was considerably lower in those plastids of Car-deficient seedlings which, after flash illumination, were kept for 1.5 h in continuous light of low intensity. The photobleaching of chlorophyll (Chl) in post-illuminated seedlings provides an indication of the photodestructive processes in Car-deficient seedlings exposed to low-intensity light. Chl bleaching did not appear in Car-deficient seedlings illuminated only with flashes; however, the stacking of the membranes was disturbed: the partition lengths and number of partitions per plastid section were higher in flashed, non-treated seedlings than in Car-deficient seedlings. Although the flashed control and NF-treated seedlings had an equal amount of Chl and the same polypeptide composition, no activity of photosystem II (PSII) and no PSII reaction centre complex were found in NF-treated seedlings. Car-deficient seedlings mainly contained photosystem I (PSI) with a ratio of Chl to P700 of 60 compared with 150 in the control. It is therefore suggested that Car deficiency in flashed leaves, which may accumulate only a small amount of light-harvesting Chl ab protein, prevents the assembly of the PSII complex and membrane stacking.

Carotenoid-Induced Non-photochemical Fluorescence Quenching in Phycobilisomes of the Cyanobacterium Synechocystis sp. PCC 6803

A mechanism of carotenoid triggered quenching of phycobilisome fluorescence in a photosystem II-deficient mutant of Synechocystis sp. has been studied. The effect of temperature on quenching reveals two temperature-dependent processes: one is responsible for the quenching rate, and one determines the yield of phycobilisome fluorescence. The non-Arrhenius behavior of the light-on quenching rate suggests that carotenoidabsorbed light triggers a process that bears a strong resemblance to soluble protein folding, showing temperature-dependent enthalpy of activated complex formation. The response of phycobilisome fluorescence yield to hydration changes, and to membrane lipid phase transitions, indicates that the pool size of phycobilisome quenching depends on the state of some membrane component.