Abstract
Ascochyta lentis is a foliar pathogen of Lens species and is of worldwide importance in cultivated lentil production. High levels of resistance were identified in the wild species Lens ervoides. This resistance was explored through histopathology, qPCR estimation of fungal biomass and transcriptome sequencing in a susceptible and a resistant recombinant inbred line (RIL) of L. ervoides infected with an aggressive isolate of A. lentis. Necrotrophic growth was delayed in the resistant RIL compared to accelerated necrotrophy of A. lentis in the susceptible RIL. Analysis of the fungal secretome indicated that the early activation of cell wall-degrading enzymes contributed to increased virulence of A. lentis. On the host side, gene co-expression analysis revealed that the invasion by A. lentis caused mRNA, DNA and protein decay in infected plants regardless of the level of resistance in the host. The resistant RIL exhibited a stronger gene co-expression in lipid localization and sulfur processes, and cellular responses to nutrients and stimuli than the susceptible RIL. In addition, differential gene analysis revealed that the repression of both, gibberellin signaling and cell death associated with the hypersensitive response (HR), were associated with enhanced A. lentis resistance.
Highlights
Necrotrophic pathogens are the largest class of plant pathogens and responsible for major economic losses in a broad range of crops worldwide (Wang et al, 2014)
We found that the A. lentis transcriptomes in the susceptible LR-66-570 were separated into two groups, with one at 24 hpi, and the other at 96 and 192 hpi, which was different from the resistant LR-66-629 where three groups corresponding to 24, 96, and 192 hpi could be distinguished
From a histopathological point of view, A. lentis exhibited slower germination on, and reduced penetration and colonization into the resistant LR-66-629 than into the susceptible LR-66570. These observations were supported by quantitative PCR (qPCR) estimation of fungal biomass, revealing higher fungal biomass in LR-66570, after 96 hpi when fungal biomass significantly increased along with the aggravated leaf necrosis
Summary
Necrotrophic pathogens are the largest class of plant pathogens and responsible for major economic losses in a broad range of crops worldwide (Wang et al, 2014). When necrotrophs infect plants in a conducive ambient environment, they actively secret a variety of pathogenicity agents such as cell wall degrading enzymes, phytotoxins, extracellular polysaccharides and other disruptive enzymes to break host plant cell walls, depolarize cell membranes, disrupt plant metabolisms, inhibit protein translation, or some or all of these combined to facilitate the expansion of necrosis (Laluk and Mengiste, 2010) To fend off such an attack, a plant must correctly recognize these pathogenic strategies and appropriately respond with its immune responses to attenuate disease symptoms. It is still not clear if these strategies can be extended to all necrotrophs, as some studies reported that the increased resistances toward necrotrophs could be achieved by upregulation of R-genes and elevated salicylic acid (SA) levels which are two major components accounting for HR aggregation (Zhu et al, 2017; Kouzai et al, 2018)
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