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The novel protein CSAP accelerates leaf senescence and is negatively regulated by SAUL1 in the dark.
Plant Cell Reports ( IF 6.2 ) Pub Date : 2019-11-26 , DOI: 10.1007/s00299-019-02493-z
Won Mi So 1 , Soo Youn Kim 1, 2 , Sujin Hyoung 1 , Jeong Sheop Shin 1
Affiliation  

The chloroplast-localized protein CSAP is an ABA-responsive factor and positively regulates dark-induced senescence. This phenomenon is controlled by SAUL1 in Arabidopsis. We report here that CSAP (Chloroplast-localized Senescence-Associated Protein, AT5G39520) functions as a positive regulator of senescence and is controlled by SAUL1 (Senescence Associated E3 Ubiquitin Ligase 1) in Arabidopsis. CSAP transcript level was gradually increased when senescence was progressed. Under dark conditions, the csap mutant showed delayed leaf senescence and reduced chlorophyll breakdown, but overexpression of CSAP accelerated leaf senescence and expressions of chlorophyll catabolic genes were up-regulated compared to the wild-type (WT). NCED3 and AAO3, which are involved in ABA biosynthesis, also showed higher expression in the overexpression lines than the WT. It is known that the CSAP transcript is increased in the saul1 mutant that shows precocious senescence. In our experiments, we confirmed that CSAP interacts with SAUL1 by the yeast two-hybrid and pull-down assays. In addition, we found that SAUL1 decreases the stability of CSAP in the presence of ABA. Taken together, we suggest that CSAP accelerates leaf senescence in the dark and this process is controlled by SAUL1.

中文翻译:

新型蛋白质 CSAP 加速叶片衰老,并在黑暗中受到 SAUL1 的负调控。

叶绿体定位蛋白 CSAP 是一种 ABA 反应因子,可正向调节暗诱导的衰老。这种现象是由拟南芥中的 SAUL1 控制的。我们在此报告 CSAP(叶绿体定位的衰老相关蛋白,AT5G39520)作为衰老的正调节因子,并受拟南芥中的 SAUL1(衰老相关 E3 泛素连接酶 1)控制。随着衰老的进行,CSAP 转录水平逐渐增加。在黑暗条件下, csap 突变体表现出延迟的叶片衰老和减少的叶绿素分解,但与野生型(WT)相比,CSAP 的过表达加速了叶片的衰老并且叶绿素分解代谢基因的表达上调。参与 ABA 生物合成的 NCED3 和 AAO3 在过表达系中也显示出比 WT 更高的表达。已知 CSAP 转录物在 saul1 突变体中增加,显示出早熟。在我们的实验中,我们通过酵母双杂交和下拉试验证实了 CSAP 与 SAUL1 相互作用。此外,我们发现 SAUL1 在 ABA 存在下会降低 CSAP 的稳定性。总之,我们建议 CSAP 在黑暗中加速叶片衰老,这个过程由 SAUL1 控制。
更新日期:2019-11-27
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