PINK EYE IS AN UNUSUAL PERIDERM DISORDER CHARACTERIZED BY ABERRANT SUBERIZATION: A CYTOLOGICAL ANALYSIS

Authors: Lulai, Edward; Weiland, John; Suttle, Jeffrey; SABBA, ROBERT - UNIV OF WISCONSIN-MADISON; BUSSAN, A - UNIV OF WISCONSIN-MADISON

Submitted to: American Journal of Potato Research
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 5/8/2006
Publication Date: 10/1/2006
Citation: Lulai, E.C., Weiland, J.J., Suttle, J.C., Sabba, R.P., Bussan, A.J. 2006. Pink Eye is an Unusual Periderm Disorder Characterized by Aberrant Suberization: A Cytological Analysis. American Journal of Potato Research. 83(5)409-421.

Interpretive Summary: Potato tuber Pink Eye (PE) is a disorder of unknown origin that results in significant postharvest quality deterioration and rot. Little is known about the physiology of PE, including the source of the characteristic tissue autofluorescence that defines the PE syndrome. The objective of this research was to identify the source of PE induced autofluorescence and PE related susceptibility to infection. The suberized cells of the native periderm, located at the tuber surface, and the induction of suberization on other cell walls were investigated to determine their role in the PE disorder. Suberin is composed of two major biopolymers. Suberin poly(phenolics) (SPP) are attached to the cell walls and protect against bacterial infection. Suberin poly(aliphatics) (SPA) are bonded via a glycerol linkage to the SPP and provide a barrier to fungal infection. The results showed that the integrity of the native periderm was compromised or in some places absent in PE tubers. The PE complex was defined by unusual SPP accumulations inside the tuber in the cortical parenchyma followed by latent SPA accumulations. The SPA accumulations were generally insufficient to form a complete barrier that was competent to block infections by pathogenic bacteria and fungi. The absence or compromised integrity of the suberin barrier and its associated waxes resulted in increased susceptibility to water vapor loss which is know to cause tuber shrinkage and flaccidity. Widespread accumulations of SPP on parenchyma cell walls were found to be the source of autofluorescence commonly used to determine the presence of the disorder. These results are of critical importance because they are the first to: (1) determine the source of PE induced autofluorescence that defines the presence of the disorder, (2) implicate the breakdown of the native periderm and its associated suberin barrier with the PE complex and the susceptibility of PE tubers to pathogen infection, (3) visually illustrate how the PE induced deterioration of tuber native periderm may lead to fungal infection(s) that can only be blocked by internal accumulation of both SPP and SPA, and (4) provide evidence that PE is a physiological disorder. Collectively, this research creates a new physiologically based model for PE which clearly shows that a compromised suberin barrier and aberrant suberization are pivotal to the disorder and susceptibility to infection. The model/results explain why a causal organism for PE could not be found in earlier research and may be used to develop science-based and targeted management tools for this disorder.

Technical Abstract: Potato tuber Pink Eye (PE) is a disorder of unknown origin that results in significant postharvest quality deterioration and rot. Little is known about the physiology of PE, including the characteristic tissue autofluorescence that defines the PE syndrome. The objective of this research was to identify the source of PE induced autofluorescence and PE related susceptibility to infection. The suberized barrier of the native periderm and suberization of neighboring tissues were investigated to determine their role in the PE disorder. The results showed that the integrity of the suberized domain of native periderm was compromised or in some places absent in PE tubers. The PE complex was defined by unusual suberin poly(phenolic) (SPP) accumulations in the cortical parenchyma followed by latent suberin poly(aliphatic) (SPA) accumulations that were generally insufficient to form a complete barrier that was competent to block infections by pathogenic bacteria and fungi. These deteriorations and deficiencies generally started at the bud end of the tuber, leaving these and other afflicted areas where the syndrome was expressed without a comprehensive barrier to infection. The absence or compromised integrity of the suberin barrier, and putatively its associated waxes, resulted in increased susceptibility to water vapor loss known to cause tuber shrinkage and flaccidity. Widespread accumulations of SPP on parenchyma cell walls were found to be the source of autofluorescence commonly used to determine the presence of the disorder. These results are of critical importance because they are the first to: (1) determine the source of PE induced autofluorescence that defines the presence of the disorder, (2) implicate the breakdown of the native periderm and its associated suberin barrier with PE and the susceptibility of PE tubers to pathogen infection, (3) demonstrate the interior development of PE induced suberin closing layers along with the latent or absent accumulation of SPA, (4) visually illustrate how the PE induced deterioration of tuber native periderm may lead to fungal infection that can only be blocked by internal accumulation of both SPP and SPA, (5) provide evidence that PE is a physiological disorder, (6) demonstrate a non-rotting fungal infection, Rhizoctonia solani, in cortical tissues of a PE sample which may be used as an example within this new paradigm to explain the PE infection court and rot anomalies and (7) demonstrate that neutral red may be used as a sensitive fluorochrome to detect intact hydrophobic areas in hyphae.