Abstract
Melampsora larici-populina causes serious poplar foliar diseases called rust worldwide. Salicylic acid (SA) and jasmonic acid (JA) are important phytohormones that are related to plant defence responses. To investigate the transcriptome profiles of SA- and JA-related genes involved in poplar rust interaction, two tolerant poplars and one intolerant poplar were selected for this study. Weighted gene coexpression network analysis (WGCNA) was applied to characterize the changes in the transcriptome profiles and contents of SA and JA after infection with the virulent E4 race of M. larici-populina. In response to infection with the E4 race of M. larici-populina, tolerant symptoms were correlated with the expression of genes related to SA and JA biosynthesis, the levels of SA and JA, and the expression of defence-related genes downstream of SA and JA. Tolerant poplars could promptly regulate the occurrence of defence responses by activating or inhibiting SA or JA pathways in a timely manner, including regulating the expression of genes related to programmed cell death, such as Kunitz-type trypsin inhibitor (KTI), to limit the growth of E4 and protect themselves. WGCNA suggested that KTI might be regulated by a Cytochrome P450 family (CYP) gene. Some CYPs should play an important role in both JA- and SA-related pathways. In contrast, in intolerant poplar, the inhibition of SA-related defence signalling through increasing JA levels in the early stage led to continued inhibition of a large number of plant–pathogen interaction-related and signalling-related genes, including NBS-LRRs, EDS1, NDR1, WRKYs, and PRs. Therefore, timely activation or inhibition of the SA or JA pathways is the key difference between tolerant and intolerant poplars.
Highlights
Introduction published maps and institutional affilRust caused by Melampsora spp. is one of the most damaging and widely distributed diseases of poplar leaves, and the most widespread and frequent causative agent is M.larici-populina [1]
In intolerant poplar, the inhibition of Salicylic acid (SA)-related defence signalling through increasing jasmonic acid (JA) levels in the early stage led to continued inhibition of a large number of plant–pathogen interaction-related and signalling-related genes, including NBS-LRRs, EDS1, NDR1, WRKYs, and PRs
A gene homologous to allene oxide cyclase 3, chloroplastic-like (AOC, XP_011021732.1), which is involved in the production of 12-oxo-phytodienoic acid, a precursor of JA, was correlated with the free SA content and was upregulated at 2 hpi only in ‘Intolerant’ (Figure S20o), which might account for the higher JA content of ‘Intolerant’ at 2 hpi (Figure 1b). These results suggested that JA might play an important role in the early period of E4 infection, but the content of JA decreased in the later period of E4 infection, which might be beneficial to the propagation and colonization of E4
Summary
Rust caused by Melampsora spp. is one of the most damaging and widely distributed diseases of poplar leaves, and the most widespread and frequent causative agent is M. larici-populina [1]. In Europe in the mid-20th century, hybrids between Populus deltoides, P. nigra or P. trichocarpa were selected for their immunity to rust [2,3]. Breakdown of resistance to M. larici-populina in clones of these hybrids began to be detected in the early 1980s with the appearance of new races of M. larici-populina [4,5,6], and outbreaks of rust on these hybrids were caused by a new race, E4 [7]. The results of inoculation tests showed that some hybrid poplars were tolerant to infection by specific rust races. E4 can only generate a few urediniospores over a life cycle on the leaves of P. deltoides × P. trichocarpa and P. trichocarpa × P. deltoides
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