A remarkable feature of evolution of phylogroup 1 Pav is the extremely fluid nature of their T3SE repertoires. Like other

phylogroup 1 strains, the frequency of T3SE acquisition is extremely high, with 27 T3SEs acquired since it diverged from the common ancestor of the group. However, the rate of T3SE loss is much higher than has been documented for any other P. syringae strain. A total of twelve Pav BP631 T3SEs are inferred to be non-functional. CP-690550 clinical trial By comparison, the strain with the second most T3SE pseudogenes is Pto DC3000 with seven [16]. All of the pseudogenization events in Pav BP631 appear to have happened since it diverged from Pmp 302280 and Pan 302091. Indeed, seven of them involve T3SEs that were acquired since this divergence, meaning that they were either acquired as nonfunctional genes or that they became pseudogenes after acquisition. The frequency of T3SE gain and loss is much lower in the phylogroup 2 Pav strains, with six and five gains for Pav Ve013 and Pav Ve037 respectively since they diverged from other phylogroup

2 strains. This is typical of the phylogroup as a whole, with three other strains that have acquired six or less T3SEs and the largest number of T3SE gains being twelve in Ppi 1704B. Two of the Pav BP631 T3SE putative pseudogenes, avrE1 and hopM1, are notable because they are located in the CEL, which is present in all P. syringae strains with canonical hrp/hrc type III secretion systems. AvrE1 is essential for virulence in some P. syringae strains [28], but is functionally redundant with HopM1 in Pto DC3000, where it suppresses salicylic acid-mediated CP673451 purchase immunity [29]. Frameshift mutations and truncations are common in hopM1, including in Pph 1448A [8], P. syringae pv.

Selleckchem Staurosporine aptata DSM 50252 [4] and Pto T1 [10]. To date, all sequenced strains have had intact avrE1 genes, except for Psv 3335 [15], which has a contig break in the gene and Por 1_6, which has a premature stop codon, but has an intact hopM1 gene [14]. Homologs of avrE are also present in a number of other plant pathogens, including Erwinia amylovora and Pantoea stewartii, where it is essential for virulence [30–32]. Since P. syringae mutants lacking both of these T3SEs have strongly impaired virulence [33] it is unclear how Pav BP631 is able to establish infection without functional MGCD0103 datasheet copies of either gene. It is possible that HopR1 [34] or another uncharacterized T3SE compensate for the loss of AvrE and HopM1 in hazelnut. Alternatively, a low level of translation might be initiated off the highly-atypical GTA start codon in avrE[23] or another in-frame start codon might be used, though this would be likely to have drastic effects on the N-terminal secretion signal and there are no other obvious candidates for ribosome binding sites. Of the twelve putatively non-functional T3SEs in Pav BP631, four have intact homologs in phylogroup 2 Pav.