Abstract

Most photosynthetic organisms are sensitive to very high light, although acclimation mechanisms enable them to deal with exposure to strong light up to a point. Here we show that cultures of wild-type Chlamydomonas reinhardtii strain cc124, when exposed to photosynthetic photon flux density 3000 μmol m−2 s−1 for a couple of days, are able to suddenly attain the ability to grow and thrive. We compared the phenotypes of control cells and cells acclimated to this extreme light (EL). The results suggest that genetic or epigenetic variation, developing during maintenance of the population in moderate light, contributes to the acclimation capability. EL acclimation was associated with a high carotenoid-to-chlorophyll ratio and slowed down PSII charge recombination reactions, probably by affecting the pre-exponential Arrhenius factor of the rate constant. In agreement with these findings, EL acclimated cells showed only one tenth of the 1O2 level of control cells. In spite of low 1O2 levels, the rate of the damaging reaction of PSII photoinhibition was similar in EL acclimated and control cells. Furthermore, EL acclimation was associated with slow PSII electron transfer to artificial quinone acceptors. The data show that ability to grow and thrive in extremely strong light is not restricted to photoinhibition-resistant organisms such as Chlorella ohadii or to high-light tolerant mutants, but a wild-type strain of a common model microalga has this ability as well.

Highlights

  • Light is the driving force of photosynthesis and a stress factor affecting both photosystems

  • Variation within the cultures contributes to survival and growth in extreme light Transfer of C. reinhardtii cultures from photosynthetic photon flux density (PPFD) 100 to 3000 μmol m−2 s−1 led first to death of some cells, as indicated by a decrease in ­OD730 during the first 24 h in EL (Fig. 1a)

  • Isolated subpopulations were more likely to acclimate to extreme light within 96 h than cultures originating from single cells (Table 1)

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Summary

Introduction

Light is the driving force of photosynthesis and a stress factor affecting both photosystems. Photosystem II (PSII) is susceptible to light-induced damage, and the rate of damage is proportional to light intensity (Tyystjärvi and Aro 1996). Photoinhibition is counteracted by concurrent repair, and several biochemical mechanisms offer partial protection (for review, see Tyystjärvi 2013), but in spite of the protective mechanisms, light intensities far above saturation are expected to lower the number of active PSII units and thereby cause decrease in the photosynthetic rate. Mutation leading to a high-light tolerant phenotype is an obvious possible mechanism for these changes, and high-light tolerant mutants of C. reinhardtii have been isolated (Förster et al 2005; Schierenbeck et al 2015), and at least the high-light tolerant hit2-mutant has properties that enables it to tolerate photoinhibition of PSII (Virtanen et al 2019). The change is too rapid and frequent to be caused by random mutations, which prompted us to explore acclimatory changes in photoprotective mechanisms

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