Submitted to: Physiological and Molecular Plant Pathology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 4/6/2017
Publication Date: 4/30/2017
Citation: Baker, C.J., Mock, N.M., Smith, J.M., Aver'Yanov, A.A. 2017. A simplified technique to detect variations of leaf chlorogenic acid levels between and within plants caused by maturation or biological stress. Physiological and Molecular Plant Pathology. 98:97-103. doi: 10/1016/j.pmpp.2017.04.003.
Interpretive Summary: Bacterial plant diseases cause major damage to crops each year and the cost of controlling them adds greatly to production costs and often involves antibiotics which are a public concern. The plant leaf apoplast, which is the cell wall region just outside the plant cell itself, is the first line of defense against most aerial pathogens. The apoplast is much like the moat around a castle, protecting it from attack. In this manuscript we are reporting a procedure that allows us to detect when the first break in the plant cell wall occurs in pathogenic interactions. This has allowed us to differentiate between events related to early recognition versus post recognition. The leaf apoplast is highly vulnerable to manipulation either by genetic engineering or direct application of materials to leaves, via stomata or additions to ground water, and delivered by xylem. This information will benefit plant scientists and breeders who are devising new strategies to improve disease resistance in plants as well as decrease the use of chemical pesticides and antibiotics.
Technical Abstract: The composition of phenolics in the plant apoplast vary during the first 5 hr post inoculation with different bacteria, depending on the plant-bacterial interaction. In general these responsive phenolics are not found at high concentrations in the symplast, within the cell. Recently we found that in certain pathogenic interactions with tobacco, chlorogenic acids that are stored in high concentrations in the symplast vacuole, greatly increased in the apoplast after 5 to 15 hr depending on the inoculum concentration. The susceptible interaction with P.s. pv. tabaci initially had a controlled but elevated level of chlorogenic acid (CGA), which began to increase after 10 to 15 hrs. The incompatible interaction with P.s. pv. syringae (HR+) initially had low levels of CGA until 12 to 15 hr, when a large rapid increase occurred just prior to symptom development. Here we wanted to examine both symplastic and apoplastic chlorogenic acid levels during bacterial infection to determine if a physical breakdown of the apoplast/symplast barrier may be responsible for the apoplastic CGA increases. Secondarily, since most plants produce CGAs, would increases in apoplastic CGA be a measurable parameter for the detection and timing of the A/S barrier breakdown during plant/bacterial interactions.