Abstract
Maize chlorotic mottle virus (MCMV) infection causes growth abnormalities in maize. Transcriptome sequencing was conducted to compare the global gene expression of MCMV-inoculated plants with that of mock-inoculated plants. Data analyses showed that brassinosteroid (BR)-associated genes were upregulated after MCMV infection. Exogenous 2,4-epibrassinolide (BL) or brassinazole (BRZ) applications indicated that BR pathway was involved in the susceptibility to MCMV infection. In addition, treatment of BL on maize induced the accumulation of nitric oxide (NO), and the changes of NO content played positive roles in the disease incidence of MCMV. Moreover, MCMV infection was delayed when the BL-treated plants were applied with NO scavenger, which suggested that BR induced the susceptibility of maize to MCMV infection in a NO-dependent manner. Further investigation showed the maize plants with knock-down of DWARF4 (ZmDWF4, a key gene of BR synthesis) and nitrate reductase (ZmNR, a key gene of NO synthesis) by virus-induced gene silencing displayed higher resistance to MCMV than control plants. Taken together, our results suggest that BR pathway promotes the susceptibility of maize to MCMV in a NO-dependent manner.
Highlights
Plants, most of which exhibit sessile lifestyles, encounter numerous biotic and abiotic stresses, including pathogenic challenges [1]
Our research demonstrated that BR promoted the susceptibility of maize to Maize chlorotic mottle virus (MCMV) in a nitric oxide (NO)-dependent manner and provided insights into the complexity of crosstalk between plant hormones and Reactive nitrogen species (RNS) in virus-host interaction
The plants mottle on seedlings the SL1 at 7 dpi (Figure 1a) and the disease wasMCMV-inoculated over 94%
Summary
Most of which exhibit sessile lifestyles, encounter numerous biotic and abiotic stresses, including pathogenic challenges [1]. Virus invasions change host gene expression patterns, reprogram plant-signaling controls, disrupt central cellular metabolic pathways, and effectively evade defense responses leading to host susceptibility [2]. With a large diversity in virus form, replication, and pathogenic effect, it is likely that different viruses in different hosts have varied effects on plant hormone metabolism [5]. Viral infections result in hormonal disruption because of the simultaneous induction of several antagonistic hormones in susceptible plants, while these antagonistic hormones may exhibit some sequential accumulation in resistant lines [6]. Extreme severity of symptoms caused by many viruses could cause changes in hormone concentration that have no involvement the in control of the host-virus interaction, which give great prominence to the roles of hormones in plant-virus interactions [5]
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