Plant Genomic Network Research Team, RIKEN Center for Sustainable Resource Science (CSRS), Yokohama, 230-0045 Kanagawa, Japan.
Center for Bioscience Research and Education, Utsunomiya University, Utsunomiya, 321-8505 Tochigi, Japan.
Proc Natl Acad Sci U S A. 2018 May 29;115(22):5810-5815. doi: 10.1073/pnas.1719491115. Epub 2018 May 14.
Peptides encoded by small coding genes play an important role in plant development, acting in a similar manner as phytohormones. Few hormone-like peptides, however, have been shown to play a role in abiotic stress tolerance. In the current study, 17 genes coding for small peptides were found to be up-regulated in response to salinity stress. To identify peptides leading salinity stress tolerance, we generated transgenic plants overexpressing these small coding genes and assessed survivability and root growth under salinity stress conditions. Results indicated that 4 of the 17 overexpressed genes increased salinity stress tolerance. Further studies focused on , which was the most highly up-regulated gene under salinity stress. Treatment of plants with synthetic peptides encoded by revealed that a C-terminal peptide fragment (AtPep3) inhibited the salt-induced bleaching of chlorophyll in seedlings. Conversely, knockdown transgenic plants exhibited a hypersensitive phenotype under salinity stress, which was complemented by the AtPep3 peptide. This functional AtPep3 peptide region overlaps with an AtPep3 elicitor peptide that is related to the immune response of plants. Functional analyses with a receptor mutant of AtPep3 revealed that AtPep3 was recognized by the PEPR1 receptor and that it functions to increase salinity stress tolerance in plants. Collectively, these data indicate that AtPep3 plays a significant role in both salinity stress tolerance and immune response in .
由小编码基因编码的肽在植物发育中起着重要作用,其作用方式类似于植物激素。然而,很少有激素样肽被证明在非生物胁迫耐受性中发挥作用。在本研究中,发现 17 个编码小肽的基因对盐胁迫表现出上调。为了鉴定导致耐盐性的肽,我们生成了过表达这些小编码基因的转基因植物,并在盐胁迫条件下评估了它们的存活率和根生长。结果表明,在 17 个过表达基因中有 4 个提高了盐胁迫耐受性。进一步的研究集中在 AtPep3 上,它是盐胁迫下上调最显著的基因。用 AtPep3 编码的合成肽处理植物表明,C 端肽片段(AtPep3)抑制了盐诱导的幼苗中叶绿素的漂白。相反,盐胁迫下的 基因敲低转基因植物表现出超敏表型,而 AtPep3 肽可以互补这种表型。这个功能的 AtPep3 肽区域与一种与植物免疫反应相关的 AtPep3 激发肽重叠。AtPep3 的受体突变体的功能分析表明,AtPep3 被 PEPR1 受体识别,它的功能是增加植物的耐盐性。总之,这些数据表明,AtPep3 在 的盐胁迫耐受性和免疫反应中都起着重要作用。