Disruption of the 1-deoxy-D-xylulose-5-phosphate reductoisomerase (DXR) gene results in albino, dwarf and defects in trichome initiation and stomata closure in Arabidopsis
Disruption of the 1-deoxy-D-xylulose-5-phosphate reductoisomerase (DXR) gene results in albino, dwarf and defects in trichome initiation and stomata closure in Arabidopsis
复制标题
DOI：
10.1038/cr.2010.54
复制
发表时间：
2010-06-01
期刊：
影响因子：
44.1
通讯作者：
Qu, Li-Jia
中科院分区：
文献类型：
--
作者：
Xing, Shufan;Miao, Jin;Qu, Li-Jia
1-脱氧-D-木酮糖-5-磷酸还原异构酶 (DXR) 是参与 2-C-甲基-D-赤藓糖醇-4-磷酸 (MEP) 途径的重要酶，为类异戊二烯生物合成提供基本的五碳单位。为了研究 MEP 途径在植物发育和代谢中的作用，我们对 dxr 突变体 (GK_215C01) 和两个 DXR 转基因共抑制系 OX-DXR-L2 和 OX-DXR-L7 进行了详细分析。我们发现dxr突变体是白化和侏儒。它从未抽薹，毛状体的数量显着减少，并且叶子中的大多数气孔无法正常关闭。两个共抑制品系产生更多的黄色花序和没有毛状体的白化萼片。研究发现参与毛状体起始的基因的转录水平受到强烈影响，包括 GLABRA1、TRANSPARENT TESTA GLABROUS 1、TRIPTYCHON 和 SPINDLY，其表达受赤霉酸 (GA) 调节。外源应用GA3可以部分挽救dxr的矮化表型和毛状体起始，而外源应用脱落酸（ABA）可以挽救气孔闭合缺陷，表明较低水平的GA和ABA有助于dxr突变体的表型。我们进一步发现参与 GA 和 ABA 生物合成途径的基因受到协调调控。这些结果表明，质体MEP途径的破坏导致光合色素、GA和ABA的生物合成缺陷，从而导致发育异常，并且细胞质甲羟戊酸途径的通量不足以挽救质体MEP途径阻断引起的缺陷。这些结果揭示了 MEP 生物合成途径在控制类异戊二烯生物合成中的关键作用。
1-Deoxy-D-xylulose-5-phosphate reductoisomerase (DXR) is an important enzyme involved in the 2-C-methyl-D-erythritol-4-phosphate ( MEP) pathway which provides the basic five-carbon units for isoprenoid biosynthesis. To investigate the role of the MEP pathway in plant development and metabolism, we carried out detailed analyses on a dxr mutant (GK_215C01) and two DXR transgenic co-suppression lines, OX-DXR-L2 and OX-DXR-L7. We found that the dxr mutant was albino and dwarf. It never bolted, had significantly reduced number of trichomes and most of the stomata could not close normally in the leaves. The two co-suppression lines produced more yellow inflorescences and albino sepals with no trichomes. The transcription levels of genes involved in trichome initiation were found to be strongly affected, including GLABRA1, TRANSPARENT TESTA GLABROUS 1, TRIPTYCHON and SPINDLY, expression of which is regulated by gibberellic acids (GAs). Exogenous application of GA3 could partially rescue the dwarf phenotype and the trichome initiation of dxr, whereas exogenous application of abscisic acid (ABA) could rescue the stomata closure defect, suggesting that lower levels of both GA and ABA contribute to the phenotype in the dxr mutants. We further found that genes involved in the biosynthetic pathways of GA and ABA were coordinately regulated. These results indicate that disruption of the plastidial MEP pathway leads to biosynthetic deficiency of photosynthetic pigments, GAs and ABA, and thus the developmental abnormalities, and that the flux from the cytoplasmic mevalonate pathway is not sufficient to rescue the deficiency caused by the blockage of the plastidial MEP pathway. These results reveal a critical role for the MEP biosynthetic pathway in controlling the biosynthesis of isoprenoids.