SENESCENCE-SUPPRESSED PROTEIN PHOSPHATASE Directly Interacts with the Cytoplasmic Domain of SENESCENCE-ASSOCIATED RECEPTOR-LIKE KINASE and Negatively Regulates Leaf Senescence in Arabidopsis

SENESCENCE-SUPPRESSED PROTEIN PHOSPHATASE Directly Interacts with the Cytoplasmic Domain of SENESCENCE-ASSOCIATED RECEPTOR-LIKE KINASE and Negatively Regulates Leaf Senescence in Arabidopsis
复制标题

DOI:
10.1104/pp.15.01112
复制
发表时间:
2015-10-01
期刊:
影响因子:
7.4
通讯作者:
Wang, Ning Ning
Wang, Ning Ning
中科院分区:
生物学1区
文献类型:
--
作者:
Xiao, Dong;Cui, Yanjiao;Wang, Ning Ning

文献摘要

被引文献

相似文献

由蛋白激酶和磷酸酶介导的可逆性蛋白磷酸化在叶片衰老调控中起着重要作用。我们先前报道了富含亮氨酸的重复序列受体样激酶衰老相关受体样激酶(AtSARK)正调控拟南芥(Arabidopsis thaliana)叶片衰老。在这里,我们报告的参与蛋白丝氨酸/苏氨酸磷酸酶2C型蛋白磷酸酶,衰老抑制蛋白磷酸酶(SSPP),在拟南芥叶片衰老的负调控。SSPP转录水平在自然衰老和SARK诱导的早衰过程中均显著下降。过表达SSPP显著延缓拟南芥叶片衰老。蛋白质下拉和双分子荧光互补分析表明,定位于胞质溶胶的SSPP可以与质膜定位的AtSARK的胞质结构域相互作用。体外实验表明,SSPP具有蛋白磷酸酶功能,可使AtSARK胞浆结构域去磷酸化。与这些观察结果相一致,SSPP的过表达有效地挽救了AtSARK诱导的早熟叶片衰老和激素反应的变化。这些结果表明,SSPP通过抑制或干扰SARK介导的衰老信号转导,维持叶片正常寿命,防止叶片早衰。
Reversible protein phosphorylation mediated by protein kinases and phosphatases plays an important role in the regulation of leaf senescence. We previously reported that the leucine-rich repeat receptor-like kinase SENESCENCE-ASSOCIATED RECEPTOR-LIKE KINASE (AtSARK) positively regulates leaf senescence in Arabidopsis (Arabidopsis thaliana). Here, we report the involvement of a protein serine/threonine phosphatase 2C-type protein phosphatase, SENESCENCE-SUPPRESSED PROTEIN PHOSPHATASE (SSPP), in the negative regulation of Arabidopsis leaf senescence. SSPP transcript levels decreased greatly during both natural senescence and SARK-induced precocious senescence. Overexpression of SSPP significantly delayed leaf senescence in Arabidopsis. Protein pull-down and bimolecular fluorescence complementation assays demonstrated that the cytosol-localized SSPP could interact with the cytoplasmic domain of the plasma membrane-localized AtSARK. In vitro assays showed that SSPP has protein phosphatase function and can dephosphorylate the cytosolic domain of AtSARK. Consistent with these observations, overexpression of SSPP effectively rescued AtSARK-induced precocious leaf senescence and changes in hormonal responses. All our results suggested that SSPP functions in sustaining proper leaf longevity and preventing early senescence by suppressing or perturbing SARK-mediated senescence signal transduction.