Department of Chemistry, University of California, Berkeley, CA 94720.
Molecular Biophysics and Integrated Bioimaging Division, Lawrence Berkeley National Laboratory, Berkeley, CA 94720.
Proc Natl Acad Sci U S A. 2019 Feb 26;116(9):3385-3390. doi: 10.1073/pnas.1819011116. Epub 2019 Feb 11.
Nonphotochemical quenching (NPQ) is a proxy for photoprotective thermal dissipation processes that regulate photosynthetic light harvesting. The identification of NPQ mechanisms and their molecular or physiological triggering factors under in vivo conditions is a matter of controversy. Here, to investigate chlorophyll (Chl)-zeaxanthin (Zea) excitation energy transfer (EET) and charge transfer (CT) as possible NPQ mechanisms, we performed transient absorption (TA) spectroscopy on live cells of the microalga We obtained evidence for the operation of both EET and CT quenching by observing spectral features associated with the Zea S and Zea excited-state absorption (ESA) signals, respectively, after Chl excitation. Knockout mutants for genes encoding either violaxanthin de-epoxidase or LHCX1 proteins exhibited strongly inhibited NPQ capabilities and lacked detectable Zea S and Zea ESA signals in vivo, which strongly suggests that the accumulation of Zea and active LHCX1 is essential for both EET and CT quenching in .
非光化学猝灭（NPQ）是一种光保护热耗散过程的代理，可调节光合作用的光捕获。在体内条件下，NPQ 机制及其分子或生理触发因素的鉴定一直存在争议。在这里，为了研究叶绿素（Chl）-玉米黄质（Zea）激发能转移（EET）和电荷转移（CT）作为可能的 NPQ 机制，我们对微藻的活细胞进行了瞬态吸收（TA）光谱分析。我们通过观察与 Zea S 和 Zea 激发态吸收（ESA）信号分别相关的光谱特征，获得了 EET 和 CT 猝灭作用的证据，分别在 Chl 激发后。编码类囊体叶黄素脱环氧化酶或 LHCX1 蛋白的基因敲除突变体表现出强烈抑制的 NPQ 能力，并且在体内缺乏可检测到的 Zea S 和 Zea ESA 信号，这强烈表明 Zea 和活性 LHCX1 的积累对于在 中 EET 和 CT 猝灭都是必不可少的。
