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首页> 外文期刊>Molecular and Cellular Biology >The petD gene is transcribed by functionally redundant promoters in Chlamydomonas reinhardtii chloroplasts.
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The petD gene is transcribed by functionally redundant promoters in Chlamydomonas reinhardtii chloroplasts.

机译：petD基因在莱茵衣藻叶绿体中被功能上多余的启动子转录。

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FUD6, a nonphotosynthetic mutant of Chlamydomonas reinhardtii, was previously found to be deficient in the synthesis of subunit IV of the cytochrome b6/f complex, the chloroplast petD gene product (C. Lemaire, J. Girard-Bascou, F.-A. Wollman, and P. Bennoun, Biochim. Biophys. Acta 851:229-238, 1986). The lesion in FUD6 is a 236-bp deletion between two 11-bp direct repeats in the chloroplast genome. It extends from 82 to 72 bp upstream of the 5' end of wild-type petD mRNA to 156 to 166 bp downstream of the 5' end. Thus, the deletion extends into the putative promoter and 5' untranslated region of petD. No petD mRNA of the normal size can be detected in FUD6 cells, but a low level of a dicistronic message accumulates, which contains the coding regions for subunit IV and cytochrome f, the product of the upstream petA gene. petD transcriptional activity in FUD6 is not significantly altered from the wild-type level. This transcriptional activity was eliminated by petA promoter disruptions, suggesting that it originates at the petA promoter. We conclude that the petD-coding portion of most cotranscripts is rapidly degraded in FUD6, possibly following processing events that generate the 3' end of petA mRNA. A chloroplast transformant was constructed in which only the sequence from -81 to -2 relative to the major 5' end of the petD transcript was deleted. Although this deletion eliminates all detectable petD promoter activity, the transformant grows phototrophically and accumulates high levels of monocistronic petD mRNA. We conclude that the petD gene can be transcribed by functionally redundant promoters. In the absence of a functional petD promoter, a lack of transcription termination allows the downstream petD gene to be cotranscribed with the petA coding region and thereby expressed efficiently.
机译：以前发现FUD6是莱茵衣藻的非光合作用突变体，在细胞色素b6 / f复合物叶绿体petD基因产物的IV亚基的合成中缺乏（C.Lemaire，J.Girard-Bascou，F.-A. Wollman和P.Bennoun，Biochim.Biophys.Acta 851：229-238，1986）。 FUD6中的病变是叶绿体基因组中两个11bp直接重复之间的236bp缺失。它从野生型petD mRNA 5'末端上游的82到72 bp延伸到5'末端下游的156到166 bp。因此，缺失延伸到petD的推定启动子和5'非翻译区。在FUD6细胞中未检测到正常大小的petD mRNA，但积累了少量的双顺反子信息，其中包含上游petA基因产物IV和细胞色素f的编码区。从野生型水平来看，FUD6中的petD转录活性没有明显改变。此转录活性被petA启动子破坏而消除，表明它起源于petA启动子。我们得出的结论是，大多数共转录本的petD编码部分在FUD6中迅速降解，可能是在产生petA mRNA 3'端的加工事件之后发生的。构建叶绿体转化体，其中仅删除相对于petD转录物的主要5'端的-81至-2的序列。尽管此删除消除了所有可检测到的petD启动子活性，但该转化株光养生长并积累了高水平的单顺反子petD mRNA。我们得出结论，可以通过功能上多余的启动子转录petD基因。在没有功能性petD启动子的情况下，转录终止的缺乏使下游petD基因与petA编码区共转录，从而有效表达。

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