Differentiation of Verticillium dahliae populations on the basis of vegetative compatibility and pathogenicity on cotton

Abstract Complementary auxotrophic nitrate-nonutilizing (nit) mutants were used to investigate vegetative compatibility within 27 strains of Verticillium dahliae isolated from several hosts originating from Africa, Asia, Europe and the United States. Using about 500 nit mutants generated from these strains, three vegetative compatibility groups, 1 , 2 and 4, were identified. Simultaneously, virulence of each strain was assessed on cultivars of Gossypium hirsutum, G. barbadense and G. arboreum, based upon Foliar Alteration Index (FAI) and Browning Index (BI) estimation. The strains in VCGl were of both the cottondefoliating pathotype and race 3 (on cotton) but were non pathogenic on tomato; those in VCG2 and VCG4 were of the nondefoliating pathotype and belonged to different races on cotton and on tomato. Hyaline mutants deriving from parental wild-type strain showed differences in pathogenicity but were always assigned to the parental VCG. A relationship was established between VCGs and the taxonomic position of host plants. Data from nit pairings indicated that the sub-populations of V. dahliae (VCGS) may not be completely isolated genetically. .

Role of the cyclic lipopeptide massetolide A in biological control of Phytophthora infestans and in colonization of tomato plants by Pseudomonas fluorescens

Pseudomonas strains have shown promising results in biological control of late blight caused by Phytophthora infestans. However, the mechanism(s) and metabolites involved are in many cases poorly understood. Here, the role of the cyclic lipopeptide massetolide A of Pseudomonas fluorescens SS101 in biocontrol of tomato late blight was examined. Pseudomonas fluorescens SS101 was effective in preventing infection of tomato (Lycopersicon esculentum) leaves by P. infestans and significantly reduced the expansion of existing late blight lesions. Massetolide A was an important component of the activity of P. fluorescens SS101, since the massA-mutant was significantly less effective in biocontrol, and purified massetolide A provided significant control of P. infestans, both locally and systemically via induced resistance. Assays with nahG transgenic plants indicated that the systemic resistance response induced by SS101 or massetolide A was independent of salicylic acid signalling. Strain SS101 colonized the roots of tomato seedlings significantly better than its massA-mutant, indicating that massetolide A was an important trait in plant colonization. This study shows that the cyclic lipopeptide surfactant massetolide A is a metabolite with versatile functions in the ecology of P fluorescens SS101 and in interactions with tomato plants and the late blight pathogen P. infestans

Structural and Biochemical Changes in Salicylic-Acid-Treated Date Palm Roots Challenged with Fusarium oxysporum f. sp. albedinis

Histochemical and ultrastructural analyses were carried out to assess structural and biochemical changes in date palm roots pretreated with salicylic acid (SA) then inoculated with Fusarium oxysporum f. sp. albedinis (Foa). Flavonoids, induced proteins, and peroxidase activity were revealed in root tissues of SA-treated plants after challenge by Foa. These reactions were closely associated with plant resistance to Foa. Host reactions induced after inoculation of SA-treated plants with Foa included the plugging of intercellular spaces, the deposition of electron-dense materials at the sites of pathogen penetration, and several damages to fungal cells. On the other hand, untreated inoculated plants showed marked cell wall degradation and total cytoplasm disorganization, indicating the protective effects provided by salicylic acid in treated plants

Sources and modes of action of invasive knotweed allelopathy : the effects of leaf litter and trained soil on the germination and growth of native plants

Invasive knotweeds, native to Eastern Asia, are among the most dominant plant invaders of European and North American temperate ecosystems. Recent studies indicate that one cause of this dominance might be allelopathy, but the possible sources and modes of action of this allelopathy are insufficiently understood. Here, we asked whether the invasive knotweed Fallopia × bohemica can exert allelopathic effects on native plants also through its leaf litter, or through persistent soil contaminants, and whether these affect the germination or growth of native plants. In a germination experiment with nine native species neither litter leachate, an aqueous extract of knotweed leaves added to the soil, nor trained soil with a history of Fallopia pre-cultivation suppressed the germination or early growth of natives. A mesocosm study with experimental native communities showed that the presence of F. × bohemica, although not a dominant in these communities, caused significant shifts of life-history strategy in two dominant natives, and that similar effects could be elicited through litter leachates or trained soil alone. However, there were hardly any effects on the biomass of natives. Our study indicates that knotweed allelopathy acts on the growth rather than germination of natives, and that soil contamination through persistent allelochemicals may not be a significant problem in habitat restoration. It also shows that allelopathic effects can sometimes be subtle changes in life-history and allocation patterns of the affected species

The pangenome of the wheat pathogen <i>Pyrenophora tritici-repentis</i> reveals novel transposons associated with necrotrophic effectors <i>ToxA</i> and <i>ToxB</i>

BACKGROUND: In fungal plant pathogens, genome rearrangements followed by selection pressure for adaptive traits have facilitated the co-evolutionary arms race between hosts and their pathogens. Pyrenophora tritici-repentis (Ptr) has emerged recently as a foliar pathogen of wheat worldwide and its populations consist of isolates that vary in their ability to produce combinations of different necrotrophic effectors. These effectors play vital roles in disease development. Here, we sequenced the genomes of a global collection (40 isolates) of Ptr to gain insights into its gene content and genome rearrangements. RESULTS: A comparative genome analysis revealed an open pangenome, with an abundance of accessory genes (~ 57%) reflecting Ptr’s adaptability. A clear distinction between pathogenic and non-pathogenic genomes was observed in size, gene content, and phylogenetic relatedness. Chromosomal rearrangements and structural organization, specifically around effector coding genes, were detailed using long-read assemblies (PacBio RS II) generated in this work in addition to previously assembled genomes. We also discovered the involvement of large mobile elements associated with Ptr’s effectors: ToxA, the gene encoding for the necrosis effector, was found as a single copy within a 143-kb ‘Starship’ transposon (dubbed ‘Horizon’) with a clearly defined target site and target site duplications. ‘Horizon’ was located on different chromosomes in different isolates, indicating mobility, and the previously described ToxhAT transposon (responsible for horizontal transfer of ToxA) was nested within this newly identified Starship. Additionally, ToxB, the gene encoding the chlorosis effector, was clustered as three copies on a 294-kb element, which is likely a different putative ‘Starship’ (dubbed ‘Icarus’) in a ToxB-producing isolate. ToxB and its putative transposon were missing from the ToxB non-coding reference isolate, but the homolog toxb and ‘Icarus’ were both present in a different non-coding isolate. This suggests that ToxB may have been mobile at some point during the evolution of the Ptr genome which is contradictory to the current assumption of ToxB vertical inheritance. Finally, the genome architecture of Ptr was defined as ‘one-compartment’ based on calculated gene distances and evolutionary rates. CONCLUSIONS: These findings together reflect on the highly plastic nature of the Ptr genome which has likely helped to drive its worldwide adaptation and has illuminated the involvement of giant transposons in facilitating the evolution of virulence in Ptr. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s12915-022-01433-w