<i>Pseudomonas fluorescens</i> MZ05 Enhances Resistance against <i>Setosphaeria turcica</i> by Mediating Benzoxazinoid Metabolism in the Maize Inbred Line Anke35

• Main Authors: Cheng Zhou, Zhongyou Ma, Xiaoming Lu, Lin Zhu, Congsheng Yan
• Format: Article
• Language: English
• Published: MDPI AG 2020-01-01
• Series: Agriculture
• Subjects: beneficial rhizobacteria; induced disease resistance; benzoxazinoid; <i>setosphaeria turcica</i>; dimboa
• Online Access: https://www.mdpi.com/2077-0472/10/2/32

Beneficial rhizobacteria can inhibit foliar pathogen infection by activation of defense responses, yet it the mechanisms of rhizobacteria-induced disease resistance remain largely unknown. Here, inoculation of susceptible maize plants with <i>Pseudomonas fluorescens</i> MZ05 significantly reduced disease occurrence caused by the leaf pathogen <i>Setosphaeria turcica</i>. Gene expression profiles of MZ05-inoculated plants were investigated by RNA-sequencing analyses, showing that several differentially expressed genes were positively associated with the metabolic processes of benzoxazinoids. Accordantly, the inoculation with <i>P. fluorescens</i> MZ05 resulted in a significant increase in the levels of 2,4-dihydroxy-7-methoxy-2H-1,4-benzoxazin-3(4H)-one (DIMBOA) in the maize leaves. Furthermore, pre-inoculation with <i>P. fluorescens</i> MZ05 enhanced the transcription of two defense-related marked genes <i>PAL</i> and <i>PR2a</i>, as well as <i>BX2</i> and <i>GLU2</i>, which are involved in DIMBOA biosynthesis, in pathogen-infected leaves. Defense responses in the inoculated plants were also greatly stronger and quicker than that in non-inoculated plants after pathogen attacks. However, virus-mediated silencing of <i>BX2</i> or <i>GLU2</i> remarkably attenuated the MZ05-induced effects, as evidenced by more disease occurrence and lower transcription of <i>PAL</i> and <i>PR2a</i>. Collectively, these findings indicated that the MZ05-induced increases of DIMBOA levels participated in the mediation of priming, which was the key mechanism in the rhizobacteria-induced host resistance.