American Journal of Potato Research

, Volume 82, Issue 6, pp 433–440 | Cite as

Non-wound-induced suberization of tuber parenchyma cells: A physiological response to the wilt disease pathogenVerticillium dahliae

  • Edward C. Lulai


Verticillium spp. wilt pathogens enter the root and eventually penetrate xylem vessels of the plant where they can spread into the vascular tissue of the potato tuber. Infected tuber vessel elements often become discolored creating a serious internal tuber quality defect that prevents sale of raw product to its primary market. Despite the costly losses and disease issues created by these infections, the physiological responses to colonization of tuber vessel elements are poorly described, and a model system to study these responses in the laboratory has not been developed. The objectives of this research were to develop such a model system by determining if tuber vessel elements could be infiltrated withVerticillium spp. in a laboratory setting and if a detectable physiological response could be elicited and identified. Results demonstrated that tuber vessel elements in the model system could be infiltrated and that infiltration ofVerticillium dahliae Kleb. conidia into these vessel elements induced a suberization response on the walls of neighboring parenchyma cells. However, the walls of the infiltrated tuber vessel elements did not suberize. A similar suberization response was found in tubers that had been naturally infected byVerticillium dahliae in the field. The suberization response was histochemically determined by assessing the accumulation of suberin poly(aliphatics) and poly(phenolics). This process of internal suberization of tuber parenchyma cells occurred without induction by a wound signal. Consequently, the suberization signal was derived by introduction of the plant-pathogen into the tuber vessel elements. This simple model system provides a versatile tool to investigate the physiological responses of potato tuber to colonization of vessel elements. This is believed to be the first report for such a physiological response toVerticillium spp. in potato tuber.

Additional key words

poly(phenolic) poly(aliphatic) potato suberin Solanum tuberosum


Los patógenos que causan marchitez (Verticillium spp.) ingresan a la raíz y eventualmente penetran el xilema, desde donde pueden diseminarse al tejido vascular del tubérculo de papa. Los elementos de los vasos infectados a menudo se decoloran, produciéndose un daño interno que atenta contra la calidad del tubérculo y que impide su comercialización al estado natural en el mercado primario. A pesar de las pérdidas cuantiosas a causa de estas infecciones, las respuestas fisiológicas a la colonización de los elementos vasculares del tubérculo han sido deficientemente descritas y no se ha desarrollado un sistema modelo para estudiarlas. Los objetivos de esta investigación fueron desarrollar un sistema modelo para determinar si los elementos vasculares del tubérculo pueden ser infiltrados conVerticillium spp. en un ambiente de laboratorio y si sería posible producir e identificar la respuesta fisiológica. Los resultados demostraron que los elementos de los vasos en el sistema modelo pueden ser infiltrados y que la infiltración de conidias deVerticillium dahliae Kleb indujeron una respuesta de suberización sobre las paredes de las células del parénquima vecino. Sin embargo, las paredes del sistema vascular de las células infiltradas no suberizaron. Una respuesta similar de suberización se encontró en tubérculos naturalmente infectados porV. dahliae en el campo. La respuesta de suberización ha sido histoquímicamente determinada, evaluando la acumulación de suberina polialifática y polifenólica. Este proceso de suberización interna de las células del tubérculo se produjo sin la inducción de una señal de herida. Consecuentemente la señal de suberización se derivó de la introducción del patógeno en los elementos del sistema vascular. Este simple sistema modelo proporciona una herramienta versátil para investigar las respuestas fisiológicas del tubérculo de papa a la colonización de los elementos del sistema vascular. Se cree que este es el primer reporte sobre la respuesta fisiológica de los tubérculos de papa aVerticillium spp.


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Literature cited

  1. Beckman CH. 1987. The Nature of Wilt Disease of Plants. APS Press, The American Phytopathological Society, St. Paul, MN.Google Scholar
  2. Beckman CH. 2000. Phenolic-storing cells: keys to programmed cell death and periderm formation in wilt disease resistance and in general defense responses in plants? Physiol Mol Plant Pathol 57:101–110.CrossRefGoogle Scholar
  3. Benhamou N. 1995. Ultrastructural and cytochemical aspects of the response of eggplant parenchyma cells in direct contact with Verticillium-infected xylem vessels. Physiol Mol Plant Pathol 46:321–338.CrossRefGoogle Scholar
  4. Gold J, and J Robb. 1995. The role of the coating response in Craigella tomatoes infected withVerticillium dahliae, races 1 and 2. Physiol Mol Plant Pathol 47:141–157.CrossRefGoogle Scholar
  5. Lulai EC. 2001. Tuber periderm and disease resistance.In: WR Stevenson, R Loria, GD Franc, and DP Weingartner (eds), Compendium of Potato Diseases. APS Press, The American Phytopathological Society, St. Paul, MN. pp 3–6.Google Scholar
  6. Lulai EC, and DL Corsini. 1998. Differential depositions of suberin phenolic and aliphatic domains and their roles in resistance to infection during potato tuber (Solanum tuberosum L.) wound-healing. Physiol Mol Plant Pathol 53:209–222.CrossRefGoogle Scholar
  7. Lulai EC, and WC Morgan. 1992. Histochemical probing of potato periderm with neutral red: a sensitive cytofluorochrome for the hydrophobic domain of suberin. Biotech Histochem 67:185–195.PubMedCrossRefGoogle Scholar
  8. MacGuidwin AE, and DI Rouse. 1990. Role ofPratylenchus penetrans in the potato early dying disease of Russet Burbank potato. Phytopathology 80:1077–1082.CrossRefGoogle Scholar
  9. Pegg GF, and Brady BL. 2002. Verticillium Wilts. CABI Publishing, New York.Google Scholar
  10. Pennypacker BW, and KT Leath. 1986. Anatomical response of a susceptible alfalfa clone infected withVerticillium albo-atrum. Phytopathology 76:522–527.CrossRefGoogle Scholar
  11. Rowe RC, and ML Powelson. 2002. Potato early dying: management challenges in a changing production environment. Plant Dis 86:1184–1193.CrossRefGoogle Scholar
  12. Thornton RE. 2001. Vascular necrosis.In: WR Stevenson, R Loria, GD Franc, and DP Weingartner (eds), Compendium of Potato Diseases. APS Press, The American Phytopathological Society, St. Paul, MN. pp 91–92.Google Scholar
  13. Tjamos EC, RC Rowe, JB Heale, and DR Fravel. 2000. Advances in Verticillium Research and Disease Management. APS Press, The American Phytopathological Society, St. Paul, MN.Google Scholar
  14. Vaughn SF, and EC Lulai. 1991. The involvement of mechanical barriers in the resistance response of a field-resistance and a field-susceptible potato cultivar toVerticillium dahliae. Physiol Mol Plant Pathol 38:455–465.CrossRefGoogle Scholar
  15. Vaughn SF, and EC Lulai. 1992. Hypersensitive and enzyme responses in potato tuber tissue treated withVerticillium dahliae and arachidonic acid. Am Potato J 69:105–116.CrossRefGoogle Scholar

Copyright information

© Springer 2005

Authors and Affiliations

  1. 1.USDA-ARS, Northern Crop Science LaboratoryFargoUSA

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