Innovative Institute for Plant Health, Zhongkai University of Agriculture and Engineering, Guangzhou, 510225, People's Republic of China; Department of Plant Breeding and Genetics, Ghazi University, Dera Ghazi Khan, Pakistan.
Department of Botany, Government College University, Faisalabad, Pakistan.
Microb Pathog. 2021 Jul;156:104909. doi: 10.1016/j.micpath.2021.104909. Epub 2021 May 6.
Pepper's (Capsicum annum) response to bacterial pathogen Ralstonia solanacearm inoculation (RSI) and abiotic stresses is known to be synchronized by transcriptional network; however, related molecular mechanisms need extensive experimentation. We identified and characterized functions of CabHLH113 -a basic helix-loop-helix transcription factor-in pepper immunity to R. solanacearum infection. The RSI and foliar spray of phytohormones, including salicylic acid (SA), methyl jasmonate (MeJA), ethylene (ETH), and absicic acid (ABA) induced transcription of CabHLH113 in pepper. Loss of function of CabHLH113 by virus-induced-gene-silencing (VIGS) compromised defense of pepper plants against RSI and suppressed relative expression levels of immunity-associated marker genes, i.e., CaPR1, CaNPR1, CaDEF1, CaHIR1 and CaABR1. Pathogen growth was significantly increased after loss of function of CabHLH113 compared with un-silenced plants with remarkable increase in pepper susceptibility. Besides, transiently over-expression of CabHLH113 induced HR-like cell death, HO accumulation and up-regulation of defense-associated marker genes, e.g. CaPR1, CaNPR1, CaDEF1, CaHIR1 and CaABR1. Additionally, transient over-expression of CabHLH113 enhanced the transcriptional levels of CaWRKY6, CaWRKY27 and CaWRKY40. Conversely, transient over-expression of CaWRKY6, CaWRKY27 and CaWRKY40 enhanced the transcriptional levels of CabHLH113. Collectively, our results indicate that newly characterized CabHLH113 has novel defense functions in pepper immunity against RSI via triggering HR-like cell death and cellular levels of defense linked genes.
辣椒(Capsicum annum)对细菌性病原体青枯菌(Ralstonia solanacearm)接种(RSI)和非生物胁迫的反应已知是由转录网络同步的;然而,相关的分子机制需要广泛的实验。我们鉴定并表征了辣椒CabHLH113-一种碱性螺旋-环-螺旋转录因子-在对青枯菌感染的免疫中的功能。RSI 和植物激素(包括水杨酸(SA)、茉莉酸甲酯(MeJA)、乙烯(ETH)和脱落酸(ABA))的叶面喷雾诱导辣椒CabHLH113的转录。通过病毒诱导的基因沉默(VIGS)功能丧失CabHLH113 削弱了辣椒植物对 RSI 的防御能力,并抑制了与免疫相关的标记基因的相对表达水平,即 CaPR1、CaNPR1、CaDEF1、CaHIR1 和 CaABR1。与未沉默的植物相比,CabHLH113 功能丧失后,病原体的生长显著增加,导致辣椒易感性显著增加。此外,CabHLH113 的瞬时过表达诱导了 HR 样细胞死亡、HO 积累和防御相关标记基因的上调,例如 CaPR1、CaNPR1、CaDEF1、CaHIR1 和 CaABR1。此外,CabHLH113 的瞬时过表达增强了 CaWRKY6、CaWRKY27 和 CaWRKY40 的转录水平。相反,CaWRKY6、CaWRKY27 和 CaWRKY40 的瞬时过表达增强了 CabHLH113 的转录水平。总之,我们的结果表明,新表征的 CabHLH113 通过触发 HR 样细胞死亡和与细胞防御相关的基因的细胞水平,在辣椒对 RSI 的免疫中具有新的防御功能。