Genetics of Plant-Pathogen Interactions Specifying Plant Disease Resistance
Open Access
- 1 January 2001
- journal article
- review article
- Published by Oxford University Press (OUP) in Plant Physiology
- Vol. 125 (1) , 73-76
Abstract
Understanding the mechanistic basis of why a certain pathogen causes disease in one host plant and not in another has long intrigued and motivated plant pathologists. Plants, in nature, are generally resistant to most pathogens. The ability of a pathogen to cause disease in a host plant is usually the exception, not the rule. This is because plants have an innate ability to recognize potential invading pathogens and to mount successful defenses. In a converse manner, successful pathogens cause disease because they are able to evade recognition or suppress host defense mechanisms or both. Since the early days of the 20th century, classical breeding for disease resistance in plants has been a major method for controlling plant diseases. However, it was not until the 1940s when H. H. Flor published his seminal work on the genetics of the interaction between flax and its obligate rust pathogen, Malamspora lini, that we gained a substantial understanding of the genetic interactions that control disease resistance in plants (10). Flor's work was novel, insightful, and under-appreciated at the time as he concurrently studied the inheritance of resistance in the host and virulence in the pathogen. This work resulted in formulation of the gene-for-gene hypothesis. In its most simple form, the gene-forgene hypothesis states that plants contain single dominant resistance (R) genes that specifically recognize pathogens that contain complementary avirulence genes. Avirulence genes can be defined as genes in the pathogen that encode a protein product that is conditionally recognized directly or indirectly only by those plants that contain the complementary R gene. Specific recognition results in the induction of defense gene expression and the inhibition of pathogen growth. However, if the plant host does not contain the R gene, the pathogen is still capable of causing disease on that plant even though it still contains the avirulence gene. It was the work of H. H. Flor that set the stage for the subsequent molecular cloning of pathogen avirulence genes and plant R genes.Keywords
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