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Summary

In just over 100 year, the focus on host-pathogen interactions in the black rot disease has shifted gradually from basic aspects of the disease cycle to enzyme production and generegulation at the molecular level. The wealth of information provided through a long history of research makes it an interesting case study. Yet, one first asks whether any one pathosystem can provide a well-rounded view of plant-microbe interactions. Although far from complete, a thorough examination of a single bacterial disease provides a framework for deciphering the language of host-pathogen signalling mechanisms. To understand this system in depth, we take a broad overview of the disease, the pathogen and its natural variability. Then beginning with initial inoculum and epiphytic colonization we consider the steps in breaching a seeries of physical and chemical barriers, responding to the ionic environment, and appropriating nutrients within plant tissues. What attracts the pathogen to the hydathodes at leaf margins? And once having penetrated natural openings, what factors contribute to its movement through the epithem and into the xylem? What enables the black rot pathogen to invade xylame elements whereas closely related leaf spot pathogens are restricted to mesophyll tissues of the same hosts? What triggers the host response? What genes are responsible and how are they regulated? Are these genes interchangeable among pathogens? How have these questions been approached experimentally, and what is now known about them? What are the next steps? A historical perspective is interspersed in this chapter because it provides significant information leading to our current understanding of black rot as a model disease and deepens our comprehension of host-pathogen interactions. Finally, brief comparisons with several other diseases caused by bacteria in the genus. Xanthomonas is made in the attempt to find appropriate areas for generalization.

“In July, 1889, cabbage in the vicinity of Lexington was badly affected with a rot, which bore marks of being caused by the bacteria in the tissue. In some gardens two-thirds of the heads were affected, and of these more than half were completely invaded and rendered worthless… The invaded leaves became brown and watery at first; later, to become black as the decay had reached an advanced stage. The heads…gave forth a peculiarly noxious odor such as cabbage alone among vegetables is capable of producing. This final rotting was doubtless ordinary decomposition brought about by septic bacteria… it seems to me we have here a well-marked disease of cabbage… attributable, perhaps, to several causes working together, and at least encouraged by the vital activities of bacteria… it is only during periods of high temperature and excessive rainfall that the organisms are able to invade and break down the tissues of plants.” and thus proceeds the first description of black rot as observed in Lexington, Kentucky (Garman, 1890).

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Abbreviations

AF:

apoplastic fluid

Avr:

avirulence gene encoding race-specific elicitor

Ecp:

gene encoding extracellular protein

Cf:

resistance gene against Cladosporium Fulvum

GUS:

B-glucuronidase

HR:

hypersensitive response

LRR:

leucine-rich repeat

NMR:

nuclear magnetic resonance

PR:

pathogenesis-related

PVX:

potato virus X

TNF:

tumor necrosis factor

TNFR:

tumor necrosis factor receptor

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Alvarez, A.M. (2000). Black Rot of Crucifers. In: Slusarenko, A.J., Fraser, R.S.S., van Loon, L.C. (eds) Mechanisms of Resistance to Plant Diseases. Springer, Dordrecht. https://doi.org/10.1007/978-94-011-3937-3_2

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