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Evidence for proton/sulfate cotransport and its kinetics inLemna gibba G1.质子/硫酸盐共转运及其在浮萍 G1 中的动力学证据。
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Consequences of a deletion in dspA on transcript accumulation in Synechocystis sp. strain PCC6803.dspA基因缺失对聚球藻属PCC6803菌株转录积累的影响。
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PHOTOPROTECTION REVISITED: Genetic and Molecular Approaches.光保护再探讨:遗传与分子方法
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Arabidopsis CHL27, located in both envelope and thylakoid membranes, is required for the synthesis of protochlorophyllide.拟南芥CHL27位于包膜和类囊体膜中,是原叶绿素酸酯合成所必需的。
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Chlamydomonas reinhardtii genome project. A guide to the generation and use of the cDNA information.莱茵衣藻基因组计划。cDNA信息的产生与使用指南。
Plant Physiol. 2003 Feb;131(2):401-8. doi: 10.1104/pp.016899.
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The Stanford Microarray Database: data access and quality assessment tools.斯坦福微阵列数据库:数据访问与质量评估工具。
Nucleic Acids Res. 2003 Jan 1;31(1):94-6. doi: 10.1093/nar/gkg078.
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Adaptation to Fe-deficiency requires remodeling of the photosynthetic apparatus.适应缺铁环境需要对光合器官进行重塑。
EMBO J. 2002 Dec 16;21(24):6709-20. doi: 10.1093/emboj/cdf666.
8
The sac mutants of Chlamydomonas reinhardtii reveal transcriptional and posttranscriptional control of cysteine biosynthesis.莱茵衣藻的囊泡突变体揭示了半胱氨酸生物合成的转录和转录后调控。
Plant Physiol. 2002 Dec;130(4):2076-84. doi: 10.1104/pp.012484.
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Characterization of Sulfate Transport in Chlamydomonas reinhardtii during Sulfur-Limited and Sulfur-Sufficient Growth.莱茵衣藻在硫限制和硫充足生长期间硫酸盐转运的特征分析
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Selenoproteins and selenocysteine insertion system in the model plant cell system, Chlamydomonas reinhardtii.模式植物细胞系统莱茵衣藻中的硒蛋白和硒代半胱氨酸插入系统。
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基于基因表达微阵列分析对莱茵衣藻在硫饥饿期间存活情况的洞察。

Insights into the survival of Chlamydomonas reinhardtii during sulfur starvation based on microarray analysis of gene expression.

作者信息

Zhang Zhaoduo, Shrager Jeff, Jain Monica, Chang Chiung-Wen, Vallon Olivier, Grossman Arthur R

机构信息

Department of Plant Biology, The Carnegie Institute, 260 Panama St., Stanford, CA 94305, USA.

出版信息

Eukaryot Cell. 2004 Oct;3(5):1331-48. doi: 10.1128/EC.3.5.1331-1348.2004.

DOI:10.1128/EC.3.5.1331-1348.2004
PMID:15470261
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC522608/
Abstract

Responses of photosynthetic organisms to sulfur starvation include (i) increasing the capacity of the cell for transporting and/or assimilating exogenous sulfate, (ii) restructuring cellular features to conserve sulfur resources, and (iii) modulating metabolic processes and rates of cell growth and division. We used microarray analyses to obtain a genome-level view of changes in mRNA abundances in the green alga Chlamydomonas reinhardtii during sulfur starvation. The work confirms and extends upon previous findings showing that sulfur deprivation elicits changes in levels of transcripts for proteins that help scavenge sulfate and economize on the use of sulfur resources. Changes in levels of transcripts encoding members of the light-harvesting polypeptide family, such as LhcSR2, suggest restructuring of the photosynthetic apparatus during sulfur deprivation. There are also significant changes in levels of transcripts encoding enzymes involved in metabolic processes (e.g., carbon metabolism), intracellular proteolysis, and the amelioration of oxidative damage; a marked and sustained increase in mRNAs for a putative vanadium chloroperoxidase and a peroxiredoxin may help prolong survival of C. reinhardtii during sulfur deprivation. Furthermore, many of the sulfur stress-regulated transcripts (encoding polypeptides associated with sulfate uptake and assimilation, oxidative stress, and photosynthetic function) are not properly regulated in the sac1 mutant of C. reinhardtii, a strain that dies much more rapidly than parental cells during sulfur deprivation. Interestingly, sulfur stress elicits dramatic changes in levels of transcripts encoding putative chloroplast-localized chaperones in the sac1 mutant but not in the parental strain. These results suggest various strategies used by photosynthetic organisms during acclimation to nutrient-limited growth.

摘要

光合生物对硫饥饿的反应包括

(i)提高细胞运输和/或同化外源硫酸盐的能力;(ii)重构细胞特征以节约硫资源;(iii)调节代谢过程以及细胞生长和分裂的速率。我们使用微阵列分析来从基因组水平了解莱茵衣藻在硫饥饿期间mRNA丰度的变化。这项工作证实并扩展了先前的研究结果,即硫缺乏会引发有助于清除硫酸盐和节约硫资源的蛋白质转录水平的变化。编码诸如LhcSR2等捕光多肽家族成员的转录本水平的变化,表明在硫缺乏期间光合装置发生了重构。编码参与代谢过程(如碳代谢)、细胞内蛋白水解以及氧化损伤改善的酶的转录本水平也有显著变化;一种假定的钒氯过氧化物酶和一种过氧化物酶体增殖物激活受体的mRNA显著且持续增加,这可能有助于莱茵衣藻在硫缺乏期间延长存活时间。此外,许多受硫胁迫调节的转录本(编码与硫酸盐吸收和同化、氧化应激以及光合功能相关的多肽)在莱茵衣藻的sac1突变体中没有得到正确调节,该突变体在硫缺乏期间比亲本细胞死亡得更快。有趣的是,硫胁迫在sac1突变体中引发了编码假定的叶绿体定位伴侣蛋白的转录本水平的显著变化,而在亲本菌株中则没有。这些结果表明光合生物在适应营养限制生长过程中使用了各种策略。