Jean M. Bonasera

In 2014, an outbreak of soft rot disease of onion (Allium cepa) occurred in Orange County, NY. Symptoms developed following rainy, hot, humid weather and included, chlorosis, maceration of leaves, ...

Pantoea ananatis, a cause of center rot of onion, is problematic in the United States and elsewhere. The bacterium lacks disease determinants common to most other bacterial pathogens of plants. A genomic island containing the gene pepM was detected within many onion-pathogenic strains of P. ananatis of diverse origins. The pepM gene of P. ananatis putatively encodes a protein that converts phosphoenolpyruvate to phosphonopyruvate, the first step in the biosynthesis of phosphonates and related molecules. This gene appears to be essential for center rot disease. Deletion of pepM rendered the mutant strain unable to cause lesions in leaves of growing onions and water-soaking of inoculated yellow onion bulbs. Furthermore, growth of the deletion mutant in onion leaves was significantly diminished compared with wild-type bacteria, and the mutant failed to cause cell death in tobacco. Complementation of the mutated strain with pepM restored the phenotype to wild-type capability. The pepM gene is the first pathogenicity factor identified that affects bacterial fitness as well as symptom development in both leaves and bulbs in a pathogen causing center rot of onion.

Bacterial decays of onion bulbs cause sporadic and sometimes serious losses to onion (Allium cepa). In New York, three groups of bacteria were identified as problematic: Burkholderia spp., Pantoea ananatis, and Enterobacter spp. To aid in efficient detection and diagnosis of these pathogens, pairs of specific polymerase chain reaction primers were designed and validated, based on a strategy that utilized various genome sequences now available in public databases. Primer pairs were tested against numerous strains of target bacteria, closely related bacteria, and other onion-pathogenic bacteria. Each primer pair yielded a single, apparently highly specific amplicon from aqueous suspensions of the target bacteria. Minimum sensitivities were approximately 10³ CFU per 25-μl reaction mixture for all three primer pairs.

Background: In the past decade, much work has been done to dissect the molecular basis of the defence signalling pathway in plants known as Systemic Acquired Resistance (SAR). Most of the work has been carried out in model species such as Arabidopsis, with little attention paid to woody plants. However within the range of species examined, components of the pathway seem to be highly conserved. In this study, we attempted to identify downstream components of the SAR pathway in apple to serve as markers for its activation. Results: We identified three pathogenesis related (PR) genes from apple, PR-2, PR-5 and PR-8, which are induced in response to inoculation with the apple pathogen, Erwinia amylovora, but they are not induced in young apple shoots by treatment with known elicitors of SAR in herbaceous plants. We also identified three PR-1-like genes from apple, PR-1a, PR-1b and PR-1c, based solely on sequence similarity to known PR-1 genes of model (intensively researched) herbaceous plants. The PR-1-like genes were not induced in response to inoculation with E. amylovora or by treatment with elicitors; however, each showed a distinct pattern of expression. Conclusion: Four PR genes from apple were partially characterized. PR-1a, PR-2, PR-5 and PR-8 from apple are not markers for SAR in young apple shoots. Two additional PR-1-like genes were identified through in-silico analysis of apple ESTs deposited in GenBank. PR-1a, PR-1b and PR-1c are not involved in defence response or SAR in young apple shoots; this conclusion differs from that reported previously for young apple seedlings.