Transcriptome Analysis of the Melon-Fusarium oxysporum f. sp. melonis Race 1.2 Pathosystem in Susceptible and Resistant Plants

Abstract

Fusarium oxysporum f. sp. melonis Snyd. & Hans race 1.2 (FOM1.2) is the most virulent and yield-limiting pathogen of melon (Cucumis melo L.) worldwide. Current information suggest that the resistance to race 1.2 is controlled by multiple recessive genes and strongly affected by the environment. RNA-Seq analysis was used to identify candidate resistance genes and to dissect the early molecular processes deployed during melon-FOM1.2 interaction in the resistant doubled haploid line NAD and in the susceptible genotype Charentais-T (CHT) at 24 and 48 h post-inoculation (hpi). The transcriptome analysis of the NAD-FOM1.2 interaction identified 2,461 and 821 differentially expressed genes (DEGs) at 24 hpi and at 48 hpi, respectively, while in susceptible combination CHT-FOM1.2, 882 and 2,237 DEGs were recovered at 24 hpi and at 48 hpi, respectively. The overall expression profile suggests a prompt activation of the defense responses in NAD due to its basal defense-related machinery that allows an early pathogen recognition. Gene Ontology (GO) enrichment analyses revealed a total of 57 GO terms shared by both genotypes and consistent with response to fungal infection. GO classes named “chitinase activity,” “cellulase activity,” “defense response, incompatible interaction,” “auxin polar transport” emerged as major factors of resistance to FOM1.2. The data indicated that NAD reacts to FOM1.2 with a fine regulation of Ca2+-mediated signaling pathways, cell wall reorganization, and hormone crosstalk (jasmonate and ethylene, auxin and abscissic acid). Several unannotated transcripts were recovered providing a basis for a further exploration of the melon resistance genes. DEGs belonging to the FOM1.2 genome were also detected in planta as a resource for the identification of potential pathogenicity factors. This work provides a broader view of the dynamic changes of the melon transcriptome triggered by FOM1.2 and highlights that the resistance response of NAD is mainly signaled by jasmonic acid and ethylene pathways mediated by ABA and auxin. The role of candidate plant and fungal responsive genes involved in the resistance is discussed.

Combined De Novo Transcriptome and Metabolome Analysis of Common Bean Response to Fusarium oxysporum f. sp. phaseoli Infection

“…Similarly, other genes such as UDP-glucuronic acid decarboxylase and cellulose synthases were downregulated in FOP infected plants. Other genes for cell-wall reinforcement have been reported to express during FO infection in tomato [9], we also noticed a shift in expression of four proline-rich glycoprotein, four hydroxyproline-rich glycoprotein, and 18 syntaxin genes. In addition, the bean response to FOP infection 24 hpi was characterized by hyper accumulation of transcripts coding for cell-wall degradation i.e., pectate lyases, pectin methylesterase inhibitors (PMEI), pectin methylesterases (PME), and Polygalacturonases (PG) ( Table S4).…”

“…Infected plants display stunting, complete wilting, extensive chlorosis, and necrosis on the leaves [4,5]. 2 of 17 Host-F. oxysporum pathosystems have been characterized in limited crops i.e., banana (Musa paradisiaca) [6,7], melon (Cucumis melo) [8,9], chickpea (Cicer arietinum) [10][11][12], cotton (Gossypium hirsutum) [13], tomato (Lycopersicon esculentum) [14], Arabidopsis [15,16], Medicago truncatula [17]. For each plant species, the respective Fusarium pathogens and a variety of defense mechanisms have been observed, including wound responses and hypersensitive reactions as well as many gene expression and metabolic changes.…”

“…After the infection, plants recognize Fusarium oxysporum (FO) attack by understanding endogenous signals originating from the cell-wall through surveillance of cellular intactness. In this regard, many genes such as subtilin-like proteases, leucine rich-repeat proteins, proline-rice glycoproteins, cellulose synthases, and syntaxins are regulated as revealed in melon and banana [6,9,18]. In addition, constitutive enzymatic responses to FO infection appear to be important with changes in glutathione S-transferases, peroxidases, and phenylalanine ammonia lyase enzyme levels and activities being significant upon pathogen attack [19].…”

“…Identification of microbial surface derived molecules i.e., pathogen/microbe-associated molecular patterns (PAMPs/MAMPs) via pattern recognition receptors (PRRs) followed by binding of PAMPs to specific PRRs activates them and sends downstream signals to trigger broad spectrum immunity [22]. In terms of chemical defense, several genes inducing chitinases, xylem proteinases, β-1,3-glucanases thaumatin-like proteins, and peroxidases have been reported to be induced in melon against FOM infection [9]. Hypersensitive response signal molecules such as salicylic acid (SA), jasmonic acid (JA), plant growth regulating hormones, antioxidants, defense metabolites (polyphenols, phenolic acids, and flavonoids), and certain organic acids have been reported to be induced as an active plant defense [9,23].…”

“…In terms of chemical defense, several genes inducing chitinases, xylem proteinases, β-1,3-glucanases thaumatin-like proteins, and peroxidases have been reported to be induced in melon against FOM infection [9]. Hypersensitive response signal molecules such as salicylic acid (SA), jasmonic acid (JA), plant growth regulating hormones, antioxidants, defense metabolites (polyphenols, phenolic acids, and flavonoids), and certain organic acids have been reported to be induced as an active plant defense [9,23]. Certain changes at the metabolic level such as altered activity of genes involved in sugar metabolism (sucrose synthase, invertase, and β-amylase) are also considered a plant response to FO.…”