SAUR49 Can Positively Regulate Leaf Senescence by Suppressing SSPP in Arabidopsis

SAUR49 Can Positively Regulate Leaf Senescence by Suppressing SSPP in Arabidopsis
复制标题

SAUR49 可以通过抑制拟南芥中的 SSPP 来积极调节叶片衰老

DOI:
10.1093/pcp/pcz231
复制
发表时间:
2020-03-01
影响因子:
4.9
通讯作者:
Wang, Ning Ning
Wang, Ning Ning
中科院分区:
生物学2区
文献类型:
--
作者:
Wen, Zewen;Mei, Yuanyuan;Wang, Ning Ning

文献摘要

被引文献

相似文献

小生长素上调RNA(SAUR)蛋白参与叶片衰老的研究越来越受到重视,但其具体机制尚不清楚。在本研究中,我们进行了酵母双杂交试验,并确定SAUR 49作为衰老抑制蛋白磷酸酶(SSPP)的相互作用,这是一个PP 2C蛋白磷酸酶,负调控拟南芥叶片衰老通过抑制富含亮氨酸的重复序列受体样蛋白激酶衰老相关受体样激酶(SARK),如我们的小组以前报道。在植物体内进一步证实了SAUR 49与SSPP之间的相互作用。功能鉴定表明,SAUR 49是叶片衰老的正调控因子。在拟南芥叶片自然衰老过程中,SAUR 49蛋白的积累水平增加。SAUR 49的转录水平在SARK诱导的叶片早衰过程中上调,而在SSPP介导的延迟叶片衰老过程中下调。SAUR 49的过表达显著加速了拟南芥叶片的自然衰老和暗诱导衰老。更重要的是,SAUR 49过表达完全逆转了SSPP诱导的延迟叶片衰老。此外,SAUR 49的过表达逆转了SSPP介导的质膜H+ -ATP酶活性的降低。综上所述,这些结果表明SAUR 49通过抑制SSPP激活SASK介导的叶片衰老信号传导而在加速叶片衰老过程中起作用。我们进一步确定了其他四个与SSPP相互作用的SAURs,SAUR 30,SAUR 39,SAUR 41和SAUR 72,它们可能与SAUR 49在调节叶片衰老中起冗余作用。所有这些观察表明,SAUR家族的某些成员可能作为一个重要的枢纽,整合各种激素和环境信号与衰老信号在拟南芥。
The involvement of SMALL AUXIN-UP RNA (SAUR) proteins in leaf senescence has been more and more acknowledged, but the detailed mechanisms remain unclear. In the present study, we performed yeast two-hybrid assays and identified SAUR49 as an interactor of SENESCENCE SUPPRESSED PROTEIN PHOSPHATASE (SSPP), which is a PP2C protein phosphatase that negatively regulates Arabidopsis leaf senescence by suppressing the leucine-rich repeat receptor-like protein kinase SENESCENCE-ASSOCIATED RECEPTOR-LIKE KINASE (SARK), as reported previously by our group. The interaction between SAUR49 and SSPP was further confirmed in planta. Functional characterization revealed that SAUR49 is a positive regulator of leaf senescence. The accumulation level of SAUR49 protein increased during natural leaf senescence in Arabidopsis. The transcript level of SAUR49 was upregulated during SARK-induced premature leaf senescence but downregulated during SSPP-mediated delayed leaf senescence. Overexpression of SAUR49 significantly accelerated both natural and dark-induced leaf senescence in Arabidopsis. More importantly, SAUR49 overexpression completely reversed SSPP-induced delayed leaf senescence. In addition, overexpression of SAUR49 reversed the decreased plasma membrane H+ -ATPase activity mediated by SSPP. Taken together, the results showed that SAUR49 functions in accelerating the leaf senescence process via the activation of SARK-mediated leaf senescence signaling by suppressing SSPP. We further identified four other SSPP-interacting SAURs, SAUR30, SAUR39, SAUR41 and SAUR72, that may act redundantly with SAUR49 in regulating leaf senescence. All these observations indicated that certain members of the SAUR family may serve as an important hub that integrates various hormonal and environmental signals with senescence signals in Arabidopsis.