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Suppressor of Overexpression of CO 1 Negatively Regulates Dark-Induced Leaf Degreening and Senescence by Directly Repressing Pheophytinase and Other Senescence-Associated Genes in Arabidopsis

机译:通过直接抑制拟南芥中的Phosphytinase和其他与衰老相关的基因CO 1的过表达抑制剂可负调节暗诱导的叶片的衰老和衰老。

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摘要

Although the biochemical pathway of chlorophyll () degradation has been largely elucidated, how is rapidly yet coordinately degraded during leaf senescence remains elusive. Pheophytinase (PPH) is the enzyme for catalyzing the removal of the phytol group from pheophytin a, and PPH expression is significantly induced during leaf senescence. To elucidate the transcriptional regulation of PPH, we used a yeast (Saccharomyces cerevisiae) one-hybrid system to screen for its trans-regulators. SUPPRESSOR OF OVEREXPRESSION OF CO 1 (SOC1), a key flowering pathway integrator, was initially identified as one of the putative trans-regulators of PPH. After dark treatment, leaves of an SOC1 knockdown mutant (soc1-6) showed an accelerated yellowing phenotype, whereas those of SOC1-overexpressing lines exhibited a partial stay-green phenotype. SOC1 and PPH expression showed a negative correlation during leaf senescence. Substantially, SOC1 protein could bind specifically to the CArG box of the PPH promoter in vitro and in vivo, and overexpression of SOC1 significantly inhibited the transcriptional activity of the PPH promoter in Arabidopsis (Arabidopsis thaliana) protoplasts. Importantly, soc1-6 pph-1 (a PPH knockout mutant) double mutant displayed a stay-green phenotype similar to that of pph-1 during dark treatment. These results demonstrated that SOC1 inhibits degradation via negatively regulating PPH expression. In addition, measurement of the content and the maximum photochemical efficiency of photosystem II of soc1-6 and SOC1-OE leaves after dark treatment suggested that SOC1 also negatively regulates the general senescence process. Seven SENESCENCE-ASSOCIATED GENES (SAGs) were thereafter identified as its potential target genes, and NONYELLOWING1 and SAG113 were experimentally confirmed. Together, we reveal that SOC1 represses dark-induced leaf degradation and senescence in general in Arabidopsis.
机译:尽管已经阐明了叶绿素()降解的生化途径,但如何在叶衰老过程中迅速而协调地降解仍然不清楚。卟啉酶(PPH)是催化从脱镁叶绿素a中除去植醇基的酶,在叶片衰老过程中会明显诱导PPH表达。为了阐明PPH的转录调控,我们使用了酵母(Saccharomyces cerevisiae)一杂交系统来筛选其反式调控因子。 CO 1(SOC1)的过度表达的抑制因子,一种关键的开花途径整合子,最初被确定为PPH的假定反式调节因子之一。经过黑暗处理后,SOC1敲低突变体(soc1-6)的叶片显示出加速的泛黄表型,而SOC1过表达的叶片则表现出部分保持绿色的表型。 SOC1和PPH表达在叶片衰老过程中呈负相关。基本上,SOC1蛋白可以在体内和体外与PPH启动子的CArG盒特异性结合,SOC1的过表达显着抑制拟南芥(Arabidopsis thaliana)原生质体中PPH启动子的转录活性。重要的是,soc1-6 pph-1(一种PPH敲除突变体)双重突变体在黑暗处理过程中表现出与 pph-1 相似的常绿表型。这些结果表明,SOC1通过负调节 PPH 表达来抑制降解。此外,暗处理后对 soc1-6 SOC1-OE 叶片的光系统II的含量和最大光化学效率的测量表明,SOC1还负面地调节了一般衰老。处理。此后,鉴定了7个 SENESCENCE-ASSOECIATED GENES SAGs )作为其潜在的靶基因,而 NONYELLOWING1 SAG113 分别是经过实验证实。在一起,我们揭示SOC1抑制拟南芥中一般黑暗诱导的叶片降解和衰老。

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