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<p>In this study, we aimed to understand the role of cyclic electron transport (CET) in the acclimation process in response to high salinity stress by comparing wild-type <i>Chlamydomonas reinhardtii</i> with CET deficient mutants, Proton Gradient Regulation 5 (<i>PGR5</i>), and Proton Gradient Regulation Like 1 (<i>PGRL1</i>). Cells grown in photoautotrophic conditions under salt stress resulted in a primary reduction in growth and chlorophyll fluorescence, as well as OJIP transient kinetics under salt stress, indicative of diminished photochemical efficiency. Notably, all strains exhibited a decrease in the variable fluorescence, and the non-photochemical quenching was accompanied by an increase in non-regulated energy dissipation. Additionally, salt treatment resulted in a reduction in total chlorophyll content and a related increase in carotenoid levels like violaxanthin, zeaxanthin, and lutein, and these levels were more pronounced in the <i>pgr5</i>. These alterations are likely linked to enhanced reactive oxygen species (ROS) generation under salt stress. The mutants were more sensitive to ROS and showed more carotenoid content than the wild type, suggesting a compensatory photoprotective mechanism. The circular dichroism data showed that the salt stress caused changes in pigment-pigment and pigment-protein interactions, which were more significant in mutants. When cells are exposed to high salt, there is a dynamic change in the core proteins, but light-harvesting complexes and antenna proteins of photosystem (PS) I and PSII are not much affected. Further, changes in cell morphology and thylakoid membrane organization were also observed in high salt stress. These data indicate PSI remodeling, defined here as stress-induced dissociation/rearrangement of PSI–LHCI(–LHCII) super complexes, reductions in PsaA/B abundance consistent with PSI core destabilization, and loss of thylakoid macro-domain order, particularly pronounced in <i>pgr5</i>.</p>

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Investigating the role of PGR5 and PGRL1 in photosynthetic acclimation to salt stress in Chlamydomonas reinhardtii

  • 期刊论文

  • 发表日期：

    2025年11月5日

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  • Siva Naga Sai Damaraju,
  • Ranay Mohan Yadav,
  • Namrata Dubey,
  • Pavithra Ramachandran,
  • Jyoti Ranjan Rath,
  • Jerome Xavier Gunasekaran,
  • Shriya Sharma,
  • Rajagopal Subramanyam

摘要

In this study, we aimed to understand the role of cyclic electron transport (CET) in the acclimation process in response to high salinity stress by comparing wild-type Chlamydomonas reinhardtii with CET deficient mutants, Proton Gradient Regulation 5 (PGR5), and Proton Gradient Regulation Like 1 (PGRL1). Cells grown in photoautotrophic conditions under salt stress resulted in a primary reduction in growth and chlorophyll fluorescence, as well as OJIP transient kinetics under salt stress, indicative of diminished photochemical efficiency. Notably, all strains exhibited a decrease in the variable fluorescence, and the non-photochemical quenching was accompanied by an increase in non-regulated energy dissipation. Additionally, salt treatment resulted in a reduction in total chlorophyll content and a related increase in carotenoid levels like violaxanthin, zeaxanthin, and lutein, and these levels were more pronounced in the pgr5. These alterations are likely linked to enhanced reactive oxygen species (ROS) generation under salt stress. The mutants were more sensitive to ROS and showed more carotenoid content than the wild type, suggesting a compensatory photoprotective mechanism. The circular dichroism data showed that the salt stress caused changes in pigment-pigment and pigment-protein interactions, which were more significant in mutants. When cells are exposed to high salt, there is a dynamic change in the core proteins, but light-harvesting complexes and antenna proteins of photosystem (PS) I and PSII are not much affected. Further, changes in cell morphology and thylakoid membrane organization were also observed in high salt stress. These data indicate PSI remodeling, defined here as stress-induced dissociation/rearrangement of PSI–LHCI(–LHCII) super complexes, reductions in PsaA/B abundance consistent with PSI core destabilization, and loss of thylakoid macro-domain order, particularly pronounced in pgr5.