The avrRpm1 Gene of Pseudomonas syringae pv. maculicola Is Required for Virulence on Arabidopsis. Claudia Ritter. Max-Delbruck Laboratory, Carl-von-Linne Weg 10, 50829 Koln, Germany. Jeffery L. Dangl. Max-Delbruck. Laboratory, Carl-von-Linne Weg 10, 50829 Koln, Germany. MPMI 8: 444-453. Accepted 30 January 1995. Copyright 1995 The American Phytopathological Society.

We demonstrate that the avirulence gene avrRpml, isolated from Pseudomonas syringae pv. maculicola strain Psm M2 via interaction with the Arabidopsis resistance gene RPM1, is also required for maximal virulence on this host. Two avrRpml::Tn3-Spice marker-exchange mutants do not elicit a hypersensitive reaction on RPM1 -containing Arabidopsis accessions Col-0 and Oy-0. Surprisingly, these mutants neither generate disease symptoms, nor grow in planta, after inoculation onto susceptible accessions Nd-0, Fe-1, and Mt-0. These deficiencies can be corrected in a merodiploid containing a wild-type avrRpml allele, and are not observed following gene-replacement with avrRpml::Tn3-Spice alleles containing insertions just beyond the 3' terminus of the avirulence gene open reading frame. AvrRpml mRNA is expressed in low, but detectable amounts, in rich media. Induced accumulation of transcript is observed 3 h after shift to minimal media, and an avrRpml::Tn3-Spice marker-exchanged reporter gene reaches maximal induction 30 min after shift. AvrRpml transcription starts 5 base-pairs 3' of the putative regulatory "hrp-box" cis-elcment found upstream of many P. syringae avr and hrp genes. Transcriptional induction of the marker-exchanged reporter gene in minimal media is enhanced by a carbon source. Induction in planta is the same in either resistant or susceptible Arabidopsis accessions, and is unaffected by the presence or absence of wild-type avrRpml. As previously observed for many other P. syringae avr genes, transcriptional regulation of avrRpml in minimal media is dependent on hrpL and hrpS.