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酰基周转增强了集胞藻 PSII 光损伤后的恢复。

Acyl-turnover of acylplastoquinol enhances recovery of photodamaged PSII in Synechocystis.

机构信息

Department of Life Sciences, Graduate School of Arts and Sciences, The University of Tokyo, 3-8-1 Komaba, Meguro-ku, Tokyo, 153-8902, Japan.

Department of Biochemistry and Molecular Biology, Graduate School of Science and Engineering, Saitama University, 255 Shimo-Okubo, Sakura-ku, Saitama, 338-8570, Japan.

出版信息

Plant J. 2024 Nov;120(4):1317-1325. doi: 10.1111/tpj.17051. Epub 2024 Oct 10.

Abstract

Photosynthetic electron transport is carried out by the electron carrier, plastoquinone (PQ). Recently, another form of PQ, acylplastoquinol (APQ), was discovered in Synechocystis sp. PCC 6803 (Synechocystis), but its physiological function in photosynthesis is unclear. In the present study, we identified a lipase encoded in sll0482 gene in Synechocystis that deacylates APQ and releases a free fatty acid and a reduced PQ (plastoquinol, PQH), which we named acylplastoquinol lipase (APL). Disruption of apl gene increased APQ content, and recovery of photodamaged PSII under low light (LL) after the exposure to very high light (vHL) at 2500 μmol photons m sec without aeration (vHL) for 60 min, was suppressed in the Δapl cells. Δapl cells also show the slow rate of de novo synthesis of D1, a reaction center of PSII under such condition. Under high light, the cellular growth of Δapl was inhibited; however, disruption of apl gene did not affect the photosynthetic activity or photoinhibition of PSII. In wild-type cells, APQ content increased under vHL condition. Also, APQ was converted to PQH after transfer to LL with aeration by ambient air. Such striking changes in APQ were not observed in Δapl cells. The deacylation of APQ by APL may help repair PSII when PSII cannot drive photosynthetic electron transport efficiently.

摘要

光合作用电子传递由电子载体质体醌 (PQ) 进行。最近,在集胞藻 6803 (Synechocystis) 中发现了另一种形式的 PQ,酰基辅酶 Q (APQ),但其在光合作用中的生理功能尚不清楚。在本研究中,我们鉴定了集胞藻中的 sll0482 基因编码的一种脂肪酶,该酶可以使 APQ 脱酰基,释放出游离脂肪酸和还原的 PQ (质体醌,PQH),我们将其命名为酰基辅酶 Q 脂肪酶 (APL)。apl 基因的缺失增加了 APQ 的含量,并且在没有通气的情况下,经过 60 分钟 2500 μmol 光子 m sec 的非常高光 (vHL) 照射后,在低光 (LL) 下恢复光破坏的 PSII 的能力在 Δapl 细胞中受到抑制。在这种条件下,Δapl 细胞中 PSII 的 D1(反应中心)的从头合成反应也表现出较慢的速度。在高光下,Δapl 的细胞生长受到抑制;然而,apl 基因的缺失并不影响 PSII 的光合活性或光抑制。在野生型细胞中,在 vHL 条件下 APQ 含量增加。此外,APQ 在通过大气空气通气转移到 LL 时转化为 PQH。在 Δapl 细胞中未观察到 APQ 的这种明显变化。APL 对 APQ 的脱酰基作用可能有助于修复 PSII,当 PSII 不能有效地驱动光合作用电子传递时。

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