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适应缺铁环境需要对光合器官进行重塑。

Adaptation to Fe-deficiency requires remodeling of the photosynthetic apparatus.

作者信息

Moseley Jeffrey L, Allinger Tanja, Herzog Sebastian, Hoerth Patric, Wehinger Elke, Merchant Sabeeha, Hippler Michael

机构信息

Department of Chemistry and Biochemistry, UCLA, 607 Charles E. Young Drive East, Los Angeles, CA 90095-1569, USA.

出版信息

EMBO J. 2002 Dec 16;21(24):6709-20. doi: 10.1093/emboj/cdf666.

Abstract

The molecular mechanisms underlying the onset of Fe-deficiency chlorosis and the maintenance of photosynthetic function in chlorotic chloroplasts are relevant to global photosynthetic productivity. We describe a series of graded responses of the photosynthetic apparatus to Fe-deficiency, including a novel response that occurs prior to the onset of chlorosis, namely the disconnection of the LHCI antenna from photosystem I (PSI). We propose that disconnection is mediated by a change in the physical properties of PSI-K in PSI in response to a change in plastid Fe content, which is sensed through the occupancy, and hence activity, of the Fe-containing active site in Crd1. We show further that progression of the response involves remodeling of the antenna complexes-specific degradation of existing proteins coupled to the synthesis of new ones, and establishment of a new steady state with decreased stoichiometry of electron transfer complexes. We suggest that these responses are typical of a dynamic photosynthetic apparatus where photosynthetic function is optimized and photooxidative damage is minimized in graduated responses to a combination of nutrients, light quantity and quality.

摘要

缺铁性黄化病发生以及黄化叶绿体中光合功能维持的分子机制与全球光合生产力相关。我们描述了光合机构对缺铁的一系列分级反应,包括在黄化病发生之前出现的一种新反应,即光系统I(PSI)中的LHCI天线断开连接。我们提出,断开连接是由PSI中PSI-K的物理性质变化介导的,以响应质体铁含量的变化,这种变化是通过Crd1中含铁活性位点的占有率进而活性来感知的。我们进一步表明,反应的进展涉及天线复合物的重塑——现有蛋白质的特异性降解与新蛋白质的合成相结合,以及建立电子传递复合物化学计量减少的新稳态。我们认为,这些反应是动态光合机构的典型反应,在对营养、光量和光质组合的分级反应中,光合功能得到优化,光氧化损伤降至最低。

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