Key Laboratory of Potato Biology and Biotechnology, Ministry of Agriculture and Rural Affairs, Huazhong Agricultural University (HZAU), Wuhan, 430070, People's Republic of China.
Division of Plant Sciences, School of Life Science, University of Dundee (at James Hutton Institute), Errol Road, Invergowrie, Dundee, DD2 5DA, UK.
Plant Cell Rep. 2019 Feb;38(2):173-182. doi: 10.1007/s00299-018-2359-5. Epub 2018 Nov 28.
Oomycetes MAMP Pep-13 can trigger SERK3/BAK1-independent PTI. Silencing of SERK3/BAK1 in solanaceous plants resulted in reduced expression of brassinosteroid marker genes and enhanced PTI transcriptional responses to Pep-13 treatment. To prevent disease, pattern recognition receptors (PRRs) are responsible for detecting microbe-associated molecular patterns (MAMPs) to switch on plant innate immunity. SOMATIC EMBROYOGENESIS KINASE 3 (SERK3)/BRASSINOSTEROID INSENSITIVE 1-ASSOCIATED KINASE 1 (BAK1) is a well-characterized receptor-like kinase (RLK) that serves as a pivotal co-receptor with PRRs to activate immunity following recognition of MAMPs including flg22, EF-Tu, INF1 and XEG1. However, the requirement for SERK3/BAK1 in many pattern-triggered immune (PTI) signaling pathways is not yet known. Pep-13 is an oomycete MAMP that consists of a highly conserved motif (an oligopeptide of 13 amino acids) shared in Phytophthora transglutaminases. Quantitative RT-PCR analysis reveals that the transcripts of three PTI marker genes (WRKY7, WRKY8 and ACRE31) rapidly accumulate in response to three different MAMPs: flg22, chitin and Pep-13. Whereas silencing of SERK3/BAK1 in Nicotiana benthamiana or potato compromised transcript accumulation in response to flg22, it did not attenuate WRKY7, WRKY8 and ACRE31 up-regulation in response to chitin or Pep-13. This indicates that Pep-13 triggers immunity in a SERK3/BAK1-independent manner, similar to chitin. Surprisingly, silencing of SERK3/BAK1 led to significantly increased accumulation of PTI marker gene transcripts following Pep-13 or chitin treatment, compared to controls. This was accompanied by reduced expression of brassinosteroid (BR) marker genes StSTDH, StEXP8 and StCAB50 and StCHL1, which is a negative regulator of PTI, supporting previous reports that SERK3/BAK1-dependent BR signaling attenuates plant immunity. We provide Pep-13 as an alternative to chitin as a trigger of SERK3/BAK1-independent immunity.
卵菌 MAMP Pep-13 可触发 SERK3/BAK1 非依赖性 PTI。在茄科植物中沉默 SERK3/BAK1 会导致油菜素内酯标记基因的表达减少，并增强 Pep-13 处理后的 PTI 转录反应。为了预防疾病，模式识别受体 (PRR) 负责检测微生物相关分子模式 (MAMP) 以开启植物先天免疫。SOMATIC EMBRYOGENESIS KINASE 3 (SERK3)/BRASSINOSTEROID INSENSITIVE 1-ASSOCIATED KINASE 1 (BAK1) 是一种特征明确的受体样激酶 (RLK)，作为 PRR 的关键共受体，在识别包括 flg22、EF-Tu、INF1 和 XEG1 在内的 MAMP 后，可激活免疫。然而，SERK3/BAK1 在许多模式触发免疫 (PTI) 信号通路中的要求尚不清楚。Pep-13 是一种卵菌 MAMP，由植生疫霉转谷氨酰胺酶中共享的高度保守基序（由 13 个氨基酸组成的寡肽）组成。定量 RT-PCR 分析显示，三种 PTI 标记基因 (WRKY7、WRKY8 和 ACRE31) 的转录物迅速积累，以响应三种不同的 MAMP：flg22、几丁质和 Pep-13。然而，沉默 Nicotiana benthamiana 或马铃薯中的 SERK3/BAK1 会削弱对 flg22 的转录物积累，但不会减弱对几丁质或 Pep-13 的 WRKY7、WRKY8 和 ACRE31 的上调。这表明 Pep-13 以 SERK3/BAK1 非依赖性方式触发免疫，类似于几丁质。令人惊讶的是，与对照相比，沉默 SERK3/BAK1 会导致 Pep-13 或几丁质处理后 PTI 标记基因转录物的积累显著增加。这伴随着油菜素内酯 (BR) 标记基因 StSTDH、StEXP8 和 StCAB50 和 StCHL1 的表达减少，StCHL1 是 PTI 的负调节剂，支持先前的报道，即 SERK3/BAK1 依赖性 BR 信号减弱植物免疫。我们提供 Pep-13 作为替代几丁质的触发物，以触发 SERK3/BAK1 非依赖性免疫。
