The eukaryotic alga Chlamydomonas (C.) reinhardtii is used as a model organism to study photosynthetic efficiency. We studied the organization and protein profile of thylakoid membranes under severe iron (Fe²⁺) deficiency condition and iron supplement for their restoration. Chlorophyll (Chl) a fluorescence fast OJIP transients were decreased in the severe Fe²⁺ deficient cells resulting in the reduction of the photochemical efficiency. The circular dichroism (CD) results from Fe²⁺ deficient thylakoid membranes show a significant change in pigment–pigment and pigment-protein excitonic interactions. The organization of super-complexes was also affected significantly. Furthermore, super-complexes of photosystem (PS) II and PSI, along with its dimers, were severely reduced. The complexes separated using sucrose gradient centrifugation shows that loss of super-complexes and excitonic pigment-pigment interactions were restored in the severely Fe²⁺ deficient cells upon Fe supplementation for three generations. Additionally, the immunoblots demonstrated that both PSII, PSI core, and their light-harvesting complex antenna proteins were differentially decreased. However, reduced core proteins were aggregated, which in turn proteins were unfold and destabilized the supercomplexes and its function. Interestingly, the aggregated proteins were insoluble after n-Dodecyl β-D-maltoside solubilization. Further, they were identified in the pellet form. When Fe²⁺ was added to the severely deficient cells, the photosynthetic activity, pigment-proteins complexes, and proteins were restored to the level of control after 3^rd generation.

真核藻衣藻（C.）reinhardtii被用作研究光合作用效率的模型生物。我们研究了严重铁（Fe ²⁺）缺乏条件下铁质类膜的组织和蛋白质谱，并补充了铁。在严重的Fe ²⁺缺陷型细胞中，叶绿素（Chl）a的快速OJIP瞬态荧光降低，导致光化学效率降低。圆二色性（CD）来自Fe ²⁺不足的类囊体膜在色素-色素和色素-蛋白质激子相互作用中显示出显着变化。超级复合体的组织也受到显着影响。此外，光系统（PS）II和PSI的超级复合物及其二聚体也大大减少了。用蔗糖梯度离心分离的复合物表明，在重度Fe ^2+中，超级复合物的损失和激子色素-颜料的相互作用得以恢复。补铁三代后细胞缺乏。此外，免疫印迹证明PSII，PSI核心及其光捕获复杂天线蛋白均差异减少。但是，减少的核心蛋白会聚集，进而使蛋白展开并破坏超级复合物及其功能的稳定性。有趣的是，聚集的蛋白质在正十二烷基β-D-麦芽糖苷溶解后不溶。此外，它们以颗粒形式鉴定。将Fe ²⁺加入到严重缺陷细胞，所述光合活性，颜料蛋白的复合体，以及蛋白质被恢复至对照的3后的电平^RD生成。