<i>Erwinia chrysanthemi</i> genes specifically induced during infection in chicory leaves

Aguilar, Isabel; Poza‐Carrión, César; Guío, Ana; Rodrı́guez-Palenzuela, Pablo

doi:10.1046/j.1364-3703.2002.00118.x

Cited by 4 publications

(1 citation statement)

References 36 publications

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“…In vascular plants PR-1 , PAL and LOX are induced by inoculation with E.c. carotovora or by CF treatments [ 52 , 64 , 65 ] and PR-1 transcript accumulation is increased after B. cinerea infection [ 66 , 67 ]. The results obtained in this study suggest that E.c.…”

Section: Discussionmentioning

confidence: 99%

Erwinia carotovora elicitors and Botrytis cinerea activate defense responses in Physcomitrella patens

et al. 2007

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Background: Vascular plants respond to pathogens by activating a diverse array of defense mechanisms. Studies with these plants have provided a wealth of information on pathogen recognition, signal transduction and the activation of defense responses. However, very little is known about the infection and defense responses of the bryophyte, Physcomitrella patens, to well-studied phytopathogens. The purpose of this study was to determine: i) whether two representative broad host range pathogens, Erwinia carotovora ssp. carotovora (E.c. carotovora) and Botrytis cinerea (B. cinerea), could infect Physcomitrella, and ii) whether B. cinerea, elicitors of a harpin (HrpN) producing E.c. carotovora strain (SCC1) or a HrpN-negative strain (SCC3193), could cause disease symptoms and induce defense responses in Physcomitrella.

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Section: Discussionmentioning

confidence: 99%

Erwinia carotovora elicitors and Botrytis cinerea activate defense responses in Physcomitrella patens

et al. 2007

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Overexpression of Camellia sinensis Thaumatin-Like Protein, CsTLP in Potato Confers Enhanced Resistance to Macrophomina phaseolina and Phytophthora infestans Infection

et al. 2012

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Thaumatin-like proteins (TLPs), a class of pathogenesis related proteins are induced in response to pathogens and exhibit antifungal property when overexpressed in transgenic plants. In the present study, we have raised transgenic potato plants overexpressing TLP gene of Camellia sinensis (CsTLP). Fungal resistance assays of transgenic potato elucidated the potential role of CsTLP in imparting tolerance to fungal pathogens, Macrophomina phaseolina (necrotrophic) and Phytophthora infestans (hemi-biotrophic). Transgenic tubers with higher resistance to M. phaseolina, showed a concomitant and significant increase in transcripts of StPAL, StLOX, and StTLP genes involved in phenylpropanoid, lipoxygenase, and general defense response pathway, respectively after infection. Importantly, leaves of CsTLP transgenic lines inoculated with P. infestans spores under in vitro conditions also showed a resistant phenotype. The resistant phenotype recorded for the two important fungal pathogens by CsTLP transgenic potato plants is remarkable, since no effective control methods and no resistant cv. against M. phaseolina has been identified so far in potato.

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The Erwinia chrysanthemi EC16 hrp/hrc Gene Cluster Encodes an Active Hrp Type III Secretion System That Is Flanked by Virulence Genes Functionally Unrelated to the Hrp System

Rojas¹,

Ham²,

Schechter³

et al. 2004

MPMI

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Erwinia chrysanthemi is a host-promiscuous plant pathogen that possesses a type III secretion system (TTSS) similar to that of the host-specific pathogens E. amylovora and Pseudomonas syringae. The regions flanking the TTSS-encoding hrp/hrc gene clusters in the latter pathogens encode various TTSS-secreted proteins. DNA sequencing of the complete E. chrysanthemi hrp/hrc gene cluster and approximately 12 kb of the flanking regions (beyond the previously characterized hecA adhesin gene in the left flank) revealed that the E. chrysanthemi TTSS genes were syntenic and similar (>50% amino-acid identity) with their E. amylovora orthologs. However, the hrp/hrc cluster was interrupted by a cluster of four genes, only one of which, a homolog of lytic transglycosylases, is implicated in TTSS functions. Furthermore, the regions flanking the hrp/hrc cluster lacked genes that were likely to encode TTSS substrates. Instead, some of the genes in these regions predict ABC transporters and methyl-accepting chemotaxis proteins that could have alternative roles in virulence. Mutations affecting all of the genes in the regions flanking or interrupting the hrp/hrc cluster were constructed in E. chrysanthemi CUCPB5047, a mutant whose reduced pectolytic capacity can enhance the phenotype of minor virulence factors. Mutants were screened in witloof chicory leaves and then in potato tubers and Nicotiana clevelandii seedlings. Mu dII1734 insertion in one gene, designated virA, resulted in strongly reduced virulence in all three tests. virA is immediately downstream of hecA, has an unusually low G+C content of 38%, and predicts an unknown protein of 111 amino acids. The E. chrysanthemi TTSS was shown to be active by its ability to translocate AvrPto-Cya (a P. syringae TTSS effector fused to an adenylate cyclase reporter that is active in the presence of eukaryote calmodulin) into N. benthamiana leaf cells. However, VirA(1-61)-Cya was not translocated into plant cells, and virA expression was not affected by mutations in E. chrysanthemi Hrp regulator genes hrpL and hrpS. Thus, the 44-kb region of the E. chrysanthemi EC16 genome that is centered on the hrplhrc cluster encodes a potpourri of virulence factors, but none of these appear to be a TTSS effector.

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Erwinia chrysanthemi genes specifically induced during infection in chicory leaves

Cited by 4 publications

References 36 publications

Erwinia carotovora elicitors and Botrytis cinerea activate defense responses in Physcomitrella patens

Erwinia carotovora elicitors and Botrytis cinerea activate defense responses in Physcomitrella patens

Overexpression of Camellia sinensis Thaumatin-Like Protein, CsTLP in Potato Confers Enhanced Resistance to Macrophomina phaseolina and Phytophthora infestans Infection

The Erwinia chrysanthemi EC16 hrp/hrc Gene Cluster Encodes an Active Hrp Type III Secretion System That Is Flanked by Virulence Genes Functionally Unrelated to the Hrp System

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