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Shi-Kunne, X.

Publications and source records attributed to Shi-Kunne, X..

6 recordsLinked to original sources

A finished, telomere-to-telomere assembly for Botrytis cinerea strain B05.10

We present an improved genome assembly of Botrytis cinerea strain B05.10 which serves as a reference isolate for most labs active in the Botrytis research. The existing assembly dating from 2017 was extended by adding 8 telomeric regions and a small number of minor errors was corrected. The new assembly contains telomeres on each chromosome end, except for Chr4 carrying the rDNA repeat. The unannotated assembly is deposited in NCBI and manual curation of gene models is ongoing. The new assembly will be hosted on Ensembl-Fungi after completion of the structural curation.

genomics↗

Transposon activity eliminates a crucial fungal secondary metabolite cluster while preserving pathogenicity

SummaryO_LITransposable elements can significantly influence the genome dynamics of clonal fungal plant pathogens. Tropical Race 4 (TR4) is a clonal lineage within the Fusarium oxysporum species complex that poses a substantial threat to global banana production. However, how transposable elements shape TR4s genome and adaptation remains underexplored. C_LIO_LIWe investigated the activity and impact of FoHeli1, a Helitron transposable element in the TR4 lineage, focusing on a Mozambican TR4 strain (M1) through a combination of genome analyses, metabolite profiling, and infection assays. C_LIO_LIFoHeli1 activity has been very recent within the TR4 lineage and is likely still ongoing. This has resulted in large structural variations in M1, including the loss of the conserved biosynthetic gene cluster required for the production of fusaric acid. We demonstrate that this deletion abolishes fusaric acid production and alters secondary metabolite profiles, but does not affect pathogenicity. C_LIO_LIOur results emphasize the significance of transposable elements, particularly FoHeli1, in reshaping the genetic and metabolic landscape of TR4 and challenge existing assumptions about the role of fusaric acid in pathogenicity. C_LI

microbiology↗

Loss of virulence of Botrytis cinerea mutants defective in phytotoxin production is restored by modifying inoculation medium

Botrydial, botcinic acid and their derivatives are major phytotoxic metabolites produced by the necrotrophic fungal pathogen Botrytis cinerea. These phytotoxins are able to induce programmed cell death in the host and thereby promote plant susceptibility to B. cinerea. We observed that a{Delta} bot2{Delta}boa6 double mutant strain, which synthesizes neither botrydial nor botcinic acid, was almost avirulent on tomato leaves when the disease assay was performed using synthetic minimal Gamborg B5 medium. However, virulence of this mutant was restored when the inoculation medium was supplemented with yeast extract. Further virulence assays which compared the double mutant with other multiple mutants using both inoculation media, revealed a prominent contribution of botrydial and botcinic acid to the full virulence of B. cinerea. Therefore, we performed an RNA-sequencing experiment to identify B. cinerea genes that contribute to the phenotypic switch from an "incompatible" to a "compatible" interaction between tomato and the{Delta} bot2{Delta}boa6 double mutant. Four genes encoding cell death-inducing effector proteins were upregulated in B. cinerea by the addition of yeast extract, and their transcript profiles grouped within a co-expression module that was positively correlated with the compatible interaction. Functional analyses of these effector genes were performed by overexpressing them individually in the{Delta} bot2{Delta}boa6 background, followed by disease assays with the Gamborg B5 medium without yeast extract. ImportanceThe grey mould fungus Botrytis cinerea is a model for necrotrophic plant pathogens due to its wide host range, economic impact, well-assembled genome, and versatile mechanisms for inducing host cell death during colonization. Botrydial and botcinic acid have previously been characterized as major phytotoxins produced by B. cinerea. However, studies from different groups reported variable results regarding the contributions of these phytotoxins to fungal virulence. Here we demonstrate that botrydial and botcinic acid make a prominent contribution to the full virulence of B. cinerea, by performing infection assays with mutants that are defective in phytotoxin production and/or multiple cell death-inducing proteins using different inoculation media. This work highlights the pivotal roles of these phytotoxins as compared to other virulence factors, as well as the significant impact of inoculation conditions on compatible and incompatible interactions between the fungus and its hosts.

microbiology↗

Segmental Duplications Drive the Evolution of Accessory Regions in a Major Crop Pathogen

O_LIMany pathogens evolved compartmentalized genomes with conserved core and variable accessory regions which carry effector genes mediating virulence. The fungal plant pathogen Fusarium oxysporum has such accessory regions often spanning entire chromosomes. The presence of specific accessory regions influences the host range, and horizontal transfer of some accessory regions can modify the pathogenicity of the receiving strain. However, understanding how these accessory regions evolve in strains that infect the same host remains limited. C_LIO_LIHere, we define the pan-genome of 69 diverse Fusarium strains that cause Fusarium wilt of banana, a significant constraint to global banana production. In this diverse panel of Fusarium strains infecting banana, we analyzed the diversity and evolution of the accessory regions. C_LIO_LIAccessory regions in Fusarium strains infecting the same banana cultivar are highly diverse, and we could not identify any shared genomic regions and in planta induced effectors. We demonstrate that segmental duplications drive the evolution of accessory regions. Furthermore, we show that recent segmental duplications and aneuploidy occur specifically in accessory chromosomes and cause the expansion of accessory regions in F. oxysporum. C_LIO_LITaken together we conclude that extensive recent duplications drive the evolution of accessory regions in Fusarium, which contribute to the evolution of virulence. C_LI

genomics↗

Dynamic virulence-related regions of the fungal plant pathogen Verticillium dahliae display remarkably enhanced sequence conservation

Selection pressure impacts genomes unevenly, as different genes adapt with differential speed to establish an organisms optimal fitness. Plant pathogens co-evolve with their hosts, which implies continuously adaption to evade host immunity. Effectors are secreted proteins that mediate immunity evasion, but may also typically become recognized by host immune receptors. To facilitate effector repertoire alterations, in many pathogens, effector genes reside in dynamic genomic regions that are thought to display accelerated evolution, a phenomenon that is captured by the two-speed genome hypothesis. The genome of the vascular wilt pathogen Verticillium dahliae has been proposed to obey to a similar two-speed regime with dynamic, lineage-specific regions that are characterized by genomic rearrangements, increased transposable element activity and enrichment in in planta-induced effector genes. However, little is known of the origin of, and sequence diversification within, these lineage-specific regions. Based on comparative genomics among Verticillium spp. we now show differential sequence divergence between core and lineage-specific genomic regions of V. dahliae. Surprisingly, we observed that lineage-specific regions display markedly increased sequence conservation. Since single nucleotide diversity is reduced in these regions, host adaptation seems to be merely achieved through presence/absence polymorphisms. Increased sequence conservation of genomic regions important for pathogenicity is an unprecedented finding for filamentous plant pathogens and signifies the diversity of genomic dynamics in host-pathogen co-evolution.

microbiology↗

Verticillium dahliae LysM effectors differentially contribute to virulence on plant hosts

Chitin-binding LysM effectors contribute to virulence of various plant pathogenic fungi that are causal agents of foliar diseases. Here, we report on LysM effectors of the soil-borne fungal vascular wilt pathogen Verticillium dahliae. Comparative genomics revealed three core LysM effectors that are conserved in a collection of V. dahliae strains. Remarkably, and in contrast to the previously studied LysM effectors of other plant pathogens, no expression of core LysM effectors was monitored in planta in a taxonomically diverse panel of host plants. Moreover, targeted deletion of the individual LysM effector genes in V. dahliae strain JR2 did not compromise virulence in infections on Arabidopsis, tomato or Nicotiana benthamiana. Interestingly, an additional lineage-specific LysM effector is encoded in the genome of V. dahliae strain VdLs17 but not in any other V. dahliae strain sequenced to date. Remarkably, this lineage-specific effector is expressed in planta and contributes to virulence of V. dahliae strain VdLs17 on tomato, but not on Arabidopsis or on N. benthamiana. Functional analysis revealed that this LysM effector binds chitin, is able to suppress chitin-induced immune responses, and protects fungal hyphae against hydrolysis by plant hydrolytic enzymes. Thus, in contrast to the core LysM effectors of V. dahliae, this lineage-specific LysM effector of strain VdLs17 contributes to virulence in planta.

plant biology↗