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Knock-Out of the Genes Coding for the Rieske Protein and the ATP-Synthase δ-Subunit of Arabidopsis

机译:敲除拟南芥巨蛋白和aTp合成酶δ亚基的基因编码

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摘要

In Arabidopsis, the nuclear genes PetC and AtpD code for the Rieske protein of the cytochrome b6/f (cyt b6/f) complex and the δ-subunit of the chloroplast ATP synthase (cpATPase), respectively. Knock-out alleles for each of these loci have been identified. Greenhouse-grown petc-2 and atpd-1 mutants are seedling lethal, whereas heterotrophically propagated plants display a high-chlorophyll (Chl)-fluorescence phenotype, indicating that the products of PetC and AtpD are essential for photosynthesis. Additional effects of the mutations in axenic culture include altered leaf coloration and increased photosensitivity. Lack of the Rieske protein affects the stability of cyt b6/f and influences the level of other thylakoid proteins, particularly those of photosystem II. In petc-2, linear electron flow is blocked, leading to an altered redox state of both the primary quinone acceptor QA in photosystem II and the reaction center Chl P700 in photosystem I. Absence of cpATPase-δ destabilizes the entire cpATPase complex, whereas residual accumulation of cyt b6/f and of the photosystems still allows linear electron flow. In atpd-1, the increase in non-photochemical quenching of Chl fluorescence and a higher de-epoxidation state of xanthophyll cycle pigments under low light is compatible with a slower dissipation of the transthylakoid proton gradient. Further and clear differences between the two mutations are evident when mRNA expression profiles of nucleus-encoded chloroplast proteins are considered, suggesting that the physiological states conditioned by the two mutations trigger different modes of plastid signaling and nuclear response.
机译:在拟南芥中,核基因PetC和AtpD分别编码细胞色素b6 / f(cyt b6 / f)复合物的Rieske蛋白和叶绿体ATP合酶(cpATPase)的δ亚基。已经确定了每个基因座的敲除等位基因。温室种植的petc-2和atpd-1突变体对幼苗具有致命性,而异养繁殖的植物显示出高的叶绿素(Chl)-荧光表型,表明PetC和AtpD的产物对于光合作用至关重要。轴突培养中突变的其他作用包括改变叶片的颜色和增加光敏性。 Rieske蛋白的缺乏会影响cyt b6 / f的稳定性,并影响其他类囊体蛋白的水平,尤其是光系统II的类囊体蛋白的水平。在petc-2中,线性电子流被阻滞,导致光系统II中的初级醌受体QA和光系统I中的反应中心Chl P700的氧化还原状态发生变化。cpATPase-δ的存在会破坏整个cpATPase复合物的稳定性,而残留的cyt b6 / f和光系统的累积仍然允许线性电子流动。在atpd-1中,Chl荧光的非光化学猝灭的增加和叶绿素循环色素在弱光下的较高的脱环氧化状态与跨类囊体质子梯度的较慢耗散相容。当考虑细胞核编码的叶绿体蛋白的mRNA表达谱时,这两个突变之间存在明显的进一步差异,这表明由这两个突变调节的生理状态触发了质体信号传导和核反应的不同模式。

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