A salt-regulated peptide derived from the CAP superfamily protein negatively regulates salt-stress tolerance in Arabidopsis.
A salt-regulated peptide derived from the CAP superfamily protein negatively regulates salt-stress tolerance in Arabidopsis.
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DOI：
10.1093/jxb/erv263
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发表时间：
2015-08
影响因子：
6.9
通讯作者：
Chen YR
中科院分区：
文献类型：
--
作者：
Chien PS;Nam HG;Chen YR
从富含半胱氨酸的分泌蛋白之一、抗原5和致病相关1 （CAP）超家族衍生的11aa肽受盐调控，通过抑制耐盐基因赋予盐敏感性。高盐度通过改变植物的水分吸收和离子特异性毒性对植物生长产生负面影响。因此，植物进化出了一个复杂的调节网络，其中植物激素在调节对盐度的生理反应中起着重要作用。然而，目前对参与这一调控网络的植物肽的了解仍然有限。在这里，我们在拟南芥中鉴定了一种盐调节肽。该肽为11aa，来源于富含半胱氨酸的分泌蛋白、抗原5和致病相关蛋白（CAP）超家族的C端。该肽是通过使用最初被鉴定为免疫信号的番茄cap衍生肽（CAPE）前体在拟南芥中搜索同源物而发现的。为了寻找与盐反应有关的CAPE，我们筛选了具有盐反应表达的CAPE前体基因，发现PROAtCAPE1 （AT4G33730）基因受盐度调控。我们通过质谱法确认了内源性拟南芥cap衍生肽1 (AtCAPE1)，并发现PROAtCAPE1中的一个关键氨基酸残基对AtCAPE1的产生至关重要。此外，尽管PROAtCAPE1主要在根中表达，但在盐处理后，AtCAPE1被发现系统性上调。盐诱导的AtCAPE1通过抑制几个参与渗透产物产生、解毒、气孔关闭控制和细胞膜保护的耐盐基因来负向调节盐耐受性。这一发现表明，番茄免疫调节因子CAPE1的同源物AtCAPE1在盐胁迫反应的调控中发挥重要作用。因此，我们的发现表明，该肽可能在病原体防御和耐盐性之间起着权衡作用。
An 11 aa peptide derived from one of the cysteine-rich secretory proteins, antigen 5, and pathogenesis-related 1 (CAP) superfamily is salt regulated, conferring salt susceptibility through suppression of salt-tolerance genes. High salinity has negative impacts on plant growth through altered water uptake and ion-specific toxicities. Plants have therefore evolved an intricate regulatory network in which plant hormones play significant roles in modulating physiological responses to salinity. However, current understanding of the plant peptides involved in this regulatory network remains limited. Here, we identified a salt-regulated peptide in Arabidopsis. The peptide was 11 aa and was derived from the C terminus of a cysteine-rich secretory proteins, antigen 5, and pathogenesis-related 1 proteins (CAP) superfamily. This peptide was found by searching homologues in Arabidopsis using the precursor of a tomato CAP-derived peptide (CAPE) that was initially identified as an immune signal. In searching for a CAPE involved in salt responses, we screened CAPE precursor genes that showed salt-responsive expression and found that the PROAtCAPE1 (AT4G33730) gene was regulated by salinity. We confirmed the endogenous Arabidopsis CAP-derived peptide 1 (AtCAPE1) by mass spectrometry and found that a key amino acid residue in PROAtCAPE1 is critical for AtCAPE1 production. Moreover, although PROAtCAPE1 was expressed mainly in the roots, AtCAPE1 was discovered to be upregulated systemically upon salt treatment. The salt-induced AtCAPE1 negatively regulated salt tolerance by suppressing several salt-tolerance genes functioning in the production of osmolytes, detoxification, stomatal closure control, and cell membrane protection. This discovery demonstrates that AtCAPE1, a homologue of tomato immune regulator CAPE1, plays an important role in the regulation of salt stress responses. Our discovery thus suggests that the peptide may function in a trade-off between pathogen defence and salt tolerance.