PopA1, a protein which induces a hypersensitivity-like response on specific Petunia genotypes, is secreted via the Hrp pathway of Pseudomonas solanacearum.

Abstract

This paper describes the identification of a new class of extracellular bacterial proteins, typified by PopA1 and its derivative PopA3, which act as specific hypersensitive response (HR) elicitors. These two heat‐stable proteins, with HR‐like elicitor activities on tobacco (non‐host plant) but without activity on tomato (host plant), have been characterized from the supernatant of the plant pathogenic bacterium Pseudomonas solanacearum strain GMI1000. These two proteins induced the same pattern of response on Petunia, as a function of the genotypes tested. popA, the structural gene for PopA1, maps outside of the hrp gene cluster but belongs to the hrp regulon. The amino acid sequence of PopA1 does not show homology to any characterized proteins. Its secretion is dependent on hrp genes and is followed by stepwise removal of the 93 amino‐terminal amino acids, producing the protein PopA3. Petunia lines responsive to PopA3 and its precursors were resistant to infection by strain GMI1000, whereas non‐responsive lines were sensitive, suggesting that popA could be an avirulence gene. A popA mutant remained fully pathogenic on sensitive plants, indicating that this gene is not essential for pathogenicity. While lacking PopA1, this mutant, which remained avirulent on tobacco and on resistant Petunia lines, still produced additional extracellular necrogenic compounds. On the basis of both their structural features and the biological properties of the popA mutant, PopA1 and PopA3 clearly differ from hairpins characterized in other plant pathogenic bacteria.

Flagellin from an Incompatible Strain of Pseudomonas avenae Induces a Resistance Response in Cultured Rice Cells

“…One family of these proteins includes the following heat-stable, glycine-rich proteins: harpin of Erwinia amylovora (13), HrpZ pss (formally harpin pss ) of Pseudomonas syringae pv. syringae (41), and PopA of Pseudomonas (Ralstonia) solanacearum (42). Harpins and PopA were shown to elicit HR when infiltrated into the leaf laminae of the appropriate plants (13,41,42) to induce exchange of H ϩ and K ϩ across the plasma membrane (13) and to generate active oxygen species (43) when added to plant cell cultures, which are all properties of the HR elicited by live bacteria.…”

“…syringae (41), and PopA of Pseudomonas (Ralstonia) solanacearum (42). Harpins and PopA were shown to elicit HR when infiltrated into the leaf laminae of the appropriate plants (13,41,42) to induce exchange of H ϩ and K ϩ across the plasma membrane (13) and to generate active oxygen species (43) when added to plant cell cultures, which are all properties of the HR elicited by live bacteria. Recently, Felix et al (44) reported that a harpin-like protein that causes the alkalization of the tomato suspension culture medium persists in bacterial preparations of P. syringae pv.…”

A R2R3-MYB gene, AtMYB30 , acts as a positive regulator of the hypersensitive cell death program in plants in response to pathogen attack

“…Our understanding of the molecular mechanisms underlying the HR is progressing rapidly (1). Numerous data suggest that the HR is a form of programmed cell death, as its initiation depends on active plant metabolism (2,3) and can be triggered by elicitor molecules from bacteria or fungi (4)(5)(6). The overexpression of certain transgenes in plants can lead to the appearance of necrotic lesions resembling those observed during an HR (7,8).…”

The Alternative Sigma Factor RpoN Is Required for hrp Activity in Pseudomonas syringae pv. Maculicola and Acts at the Level of hrpL Transcription

“…As mentioned above, the nine hrc genes are homologous to members of the Yersinia type III secretory pathway that is responsible for translocating Yop proteins into host cells (18,24,53,73). Similarly, hrp mutations block the export of PopA1 from P. solanacearum and HrpZ (harpin) and HrpW from P. syringae, of which the latter two elicit an HR-like response on incompatible and nonhost plants (2,10,11,31). Given the role of the hrp cluster in protein secretion, the most likely cause for nonpathogenic and non-HR-eliciting phenotypes of hrp mutants is the inability to secrete a variety of virulence factors or elicitors.…”