Submitted to: Physiological and Molecular Plant Pathology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: July 1, 1998
Publication Date: N/A
Interpretive Summary: Potato tubers are easily skinned, nicked, and bruised during harvest and handling operations. Until healed, these wounds are easily infected by various bacterial and fungal pathogens that cause serious and costly rot problems for farmers, processors and consumers. We investigated the most critical biochemical phase of wound-healing known as suberization. The natural polymer suberin is synthesized on the walls of the cells neighboring the wound site and is an effective barrier to infection. We found that the two classes of biochemical compounds that make up suberin (phenolics and aliphatics) are synthesized and deposited on the cell walls at different times during wound-healing. Suberin phenolics begin to accumulate within the first 24 hr after wounding while suberin aliphatics do not begin to accumulate until three or four days after wounding. Suberin phenolics must be in place around the entire cell wall before suberin aliphatics may begin accumulating. These results are very important because suberin phenolic deposition on the first layer of wound-healing cells related directly with the development of resistance to bacterial soft rot, but had no apparent effect on resistance to fungal infection. Resistance to fungal dry rot infection began to develop as suberin aliphatics were deposited on the walls of wound-healing . Most important, total resistance to fungal infection occurred upon completion of suberin aliphatic deposition on the first layer of cells neighboring the wound.
Technical Abstract: Rapid suberization of wounded potato tubers is critical in avoiding bacterial soft rot (Erwinia carotovora carotovora, E.c.c.) and fungal dry rot (Fusarium sambucium, F.s.) infections in cut seed and stored potatoes. However until now, the reason for differential development of resistance to bacterial and then fungal penetration during suberization has not been shown to be related to the differential deposition of the two major suberin components (phenolics and aliphatics) during wound-healin bers of four varieties of diverse genetic background were wounded and inoculated with E.c.c. throughout a 5 d time course and F.s. throughout a 11 d time course during wound-healing (18 C and 98% RH). Tubers were examined at the cellular level for deposition of suberin phenolics and aliphatics, and the percent infection determined. Total resistance to infection by E.c.c. occurred after the completion of phenolic deposition on the outer tangential wall of the first layer of cells (2 to 3 d). However, this suberin phenolic matrix offered no resistance to fungal infection by F.s. even after phenolic deposition was complete on adjoining radial and inner tangential cell walls of the first layer of cells. Resistance to fungal infection did not begin to develop until the deposition of suberin aliphatics was initiated. Total resistance was attained after completion of deposition of suberin aliphatics within the first layer of suberizing cells (5 to 7 d). Results suggest separate roles for suberin phenolics and aliphatics in bacterial and fungal resistance.