Comparative anatomy of gall development on Gypsophila paniculata induced by bacteria with different mechanisms of pathogenicity

Galls induced on Gypsophila paniculata by Pantoea agglomerans pv. gypsophilae (Pag) and Agrobacterium tumefaciens (At), bacteria with different mechanisms of pathogenicity, were compared morphologically and anatomically. The pathogenicity of Pag is dependent on the presence of an indigenous plasmid...

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Bibliographic Details
Published inPlanta Vol. 224; no. 2; pp. 429 - 437
Main Authors Chalupowicz, L, Barash, I, Schwartz, M, Aloni, R, Manulis, S
Format Journal Article
LanguageEnglish
Published Berlin Springer-Verlag 01.07.2006
Springer
Springer Nature B.V
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Summary:Galls induced on Gypsophila paniculata by Pantoea agglomerans pv. gypsophilae (Pag) and Agrobacterium tumefaciens (At), bacteria with different mechanisms of pathogenicity, were compared morphologically and anatomically. The pathogenicity of Pag is dependent on the presence of an indigenous plasmid that harbors hrp gene cluster, genes encoding Hop virulence proteins and biosynthetic genes for auxin (IAA) and cytokinins (CKs), whereas that of At involves host transformation. The Pag-induced gall was rough, brittle and exhibited limited growth, in contrast to the smooth, firm appearance and continuous growth of the At-induced gall. Anatomical analysis revealed the presence of cells with enlarged nuclei and multiple nucleoli, giant cells and suberin deposition in Pag that were absent from At-induced galls. Although circular vessels were observed in both gall types, they were more numerous and the vascular system was more organized in At. An aerenchymal tissue was observed in the upper part of the galls. Ethylene emission from Pag galls, recorded 6 days after inoculation, was eight times as great as that from non-infected controls. In contrast, a significant decrease in ethylene production was observed in Gypsophila cuttings infected with Pag mutants deficient in IAA and CK production. The results presented are best accounted for by the two pathogens having distinct pathogenicity mechanisms that lead to their differential recognition by the host as non-self (Pag) and self (At).
Bibliography:http://dx.doi.org/10.1007/s00425-006-0229-9
ObjectType-Article-1
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content type line 23
ISSN:0032-0935
1432-2048
DOI:10.1007/s00425-006-0229-9