Dataset Information

Comparative transcriptome analysis of the interaction between Actinidia chinensis var. chinensis and Pseudomonas syringae pv. actinidiae in absence and presence of acibenzolar-S-methyl.

ABSTRACT: BACKGROUND:Since 2007, bacterial canker caused by Pseudomonas syringae pv. actinidiae (Psa) has become a pandemic disease leading to important economic losses in every country where kiwifruit is widely cultivated. Options for controlling this disease are very limited and rely primarily on the use of bactericidal compounds, such as copper, and resistance inducers. Among the latter, the most widely studied is acibenzolar-S-methyl. To elucidate the early molecular reaction of kiwifruit plants (Actinidia chinensis var. chinensis) to Psa infection and acibenzolar-S-methyl treatment, a RNA seq analysis was performed at different phases of the infection process, from the epiphytic phase to the endophytic invasion on acibenzolar-S-methyl treated and on non-treated plants. The infection process was monitored in vivo by confocal laser scanning microscopy. RESULTS:De novo assembly of kiwifruit transcriptome revealed a total of 39,607 transcripts, of which 3360 were differentially expressed during the infection process, primarily 3 h post inoculation. The study revealed the coordinated changes of important gene functional categories such as signaling, hormonal balance and transcriptional regulation. Among the transcription factor families, AP2/ERF, MYB, Myc, bHLH, GATA, NAC, WRKY and GRAS were found differentially expressed in response to Psa infection and acibenzolar-S-methyl treatment. Finally, in plants treated with acibenzolar-S-methyl, a number of gene functions related to plant resistance, such as PR proteins, were modulated, suggesting the set-up of a more effective defense response against the pathogen. Weighted-gene coexpression network analysis confirmed these results. CONCLUSIONS:Our work provides an in-depth description of the plant molecular reactions to Psa, it highlights the metabolic pathway related to acibenzolar-S-methyl-induced resistance and it contributes to the development of effective control strategies in open field.

SUBMITTER: Michelotti V

PROVIDER: S-EPMC6090863 | biostudies-literature | 2018 Aug

REPOSITORIES: biostudies-literature

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Comparative transcriptome analysis of the interaction between Actinidia chinensis var. chinensis and Pseudomonas syringae pv. actinidiae in absence and presence of acibenzolar-S-methyl.

Michelotti Vania V Lamontanara Antonella A Buriani Giampaolo G Orrù Luigi L Cellini Antonio A Donati Irene I Vanneste Joel L JL Cattivelli Luigi L Tacconi Gianni G Spinelli Francesco F

BMC genomics 20180806 1

<h4>Background</h4>Since 2007, bacterial canker caused by Pseudomonas syringae pv. actinidiae (Psa) has become a pandemic disease leading to important economic losses in every country where kiwifruit is widely cultivated. Options for controlling this disease are very limited and rely primarily on the use of bactericidal compounds, such as copper, and resistance inducers. Among the latter, the most widely studied is acibenzolar-S-methyl. To elucidate the early molecular reaction of kiwifruit plan ...[more]

PMID: 30081820

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Project description:Pseudomonas syringae pv. actinidiae (Psa) is a bacterial pathogen of kiwifruit. This pathogen causes leaf-spotting, cane dieback, wilting, cankers (lesions), and in severe cases, plant death. Families of diploid A. chinensis seedlings grown in the field show a range of susceptibilities to the disease with up to 100% of seedlings in some families succumbing to Psa. But the effect of selection for field resistance to Psa on the alleles that remain in surviving seedlings has not been assessed. The objective of this work was to analyse, the effect of plant removal from Psa on the allele frequency of an incomplete-factorial-cross population. This population was founded using a range of genotypically distinct diploid A. chinensis var. chinensis parents to make 28 F1 families. However, because of the diversity of these families, low numbers of surviving individuals, and a lack of samples from dead individuals, standard QTL mapping approaches were unlikely to yield good results. Instead, a modified bulk segregant analysis (BSA) overcame these drawbacks while reducing the costs of sampling and sample processing, and the complexity of data analysis. Because the method was modified, part one of this work was used to determine the signal strength required for a QTL to be detected with BSA. Once QTL detection accuracy was known, part two of this work analysed the 28 families from the incomplete-factorial-cross population that had multiple individuals removed due to Psa infection. Each family was assigned to one of eight bulks based on a single parent that contributed to the families. DNA was extracted in bulk by grinding sampled leaf discs together before DNA extraction. Each sample bulk was compared against a bulk made up of WGS data from the parents contributing to the sample bulk. The deviation in allele frequency from the expected allele frequency within surviving populations using the modified BSA method was able to identify 11 QTLs for Psa that were present in at least two analyses. The identification of these Psa resistance QTL will enable marker development to selectively breed for resistance to Psa in future kiwifruit breeding programs.

Project description:A recent re-emerging bacterial canker disease incited by Pseudomonas syringae pv. actinidiae (Psa) is causing severe economic losses to Actinidia chinensis and A. deliciosa cultivations in southern Europe, New Zealand, Chile and South Korea. Little is known about the genetic features of this pathovar. We generated genome-wide Illumina sequence data from two Psa strains causing outbreaks of bacterial canker on the A. deliciosa cv. Hayward in Japan (J-Psa, type-strain of the pathovar) and in Italy (I-Psa) in 1984 and 1992, respectively as well as from a Psa strain (I2-Psa) isolated at the beginning of the recent epidemic on A. chinensis cv. Hort16A in Italy. All strains were isolated from typical leaf spot symptoms. The phylogenetic relationships revealed that Psa is more closely related to P. s. pv. theae than to P. avellanae within genomospecies 8. Comparative genomic analyses revealed both relevant intrapathovar variations and putative pathovar-specific genomic regions in Psa. The genomic sequences of J-Psa and I-Psa were very similar. Conversely, the I2-Psa genome encodes four additional effector protein genes, lacks a 50 kb plasmid and the phaseolotoxin gene cluster, argK-tox but has acquired a 160 kb plasmid and putative prophage sequences. Several lines of evidence from the analysis of the genome sequences support the hypothesis that this strain did not evolve from the Psa population that caused the epidemics in 1984-1992 in Japan and Italy but rather is the product of a recent independent evolution of the pathovar actinidiae for infecting Actinidia spp. All Psa strains share the genetic potential for copper resistance, antibiotic detoxification, high affinity iron acquisition and detoxification of nitric oxide of plant origin. Similar to other sequenced phytopathogenic pseudomonads associated with woody plant species, the Psa strains isolated from leaves also display a set of genes involved in the catabolism of plant-derived aromatic compounds.

Dataset Information

Comparative transcriptome analysis of the interaction between Actinidia chinensis var. chinensis and Pseudomonas syringae pv. actinidiae in absence and presence of acibenzolar-S-methyl.

Publications

Comparative transcriptome analysis of the interaction between Actinidia chinensis var. chinensis and Pseudomonas syringae pv. actinidiae in absence and presence of acibenzolar-S-methyl.

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