The potato late blight pathogen, known to scientists as Phytophthora infestans, is a fungus-like organism that was responsible for the Irish Potato Famine of the 1840s and continues to cause devastating agricultural losses worldwide today. Infected plants are characterized by dark lesions on the stems, leaves, and tubers; damage to the tuber surface allows other fungi and bacteria to enter and destroy the core, often resulting in a foul odor. P. infestans is related to approximately 65 other pathogens that cause similar damage to commercial crops as well as natural vegetation.
In the potato-Phytophthora system, the host-pathogen response has evolved in a highly specific way: resistance (R) genes from wild species, which are introduced into cultivated potato by breeding, are matched by avirulence (Avr) genes in Phytophthora. While many such gene matches are predicted, only a few have been confirmed by molecular and functional studies. Avr genes are thought to undergo rapid changes to evade detection by plants that possess R genes, which means that many strains of Phytophthora and potato are likely to be evolving at the present time.
"P. infestans is notorious for its ability to change in response to R g enes," says Dr. Francine Govers, the principal investigator on the project. "These changes are probably facilitated by its underlying genomic plasticity. Field isolates of P. infestans are known to be genetically highly variable."
Govers, along with colleagues Rays Jiang, Rob Weide, and Peter van de Vondervoort, set out to identify the genetic basis for the virulence of specific Dutch P. infestans strains. The outcome of their efforts was the identification of single gene, called pi3.4, that was present as a single, full-length copy in both the virulent and avirulent strains. They also identified multiple copies of pi3.4 only in the avirulent strain ?but, interestingly, these copies represented only part of the pi3.4 gene.
The authors speculate that the partial gene copies could function as a source of modules for generating new genes. These new genes could be produced by unequal crossing-over, or exchange of genetic material, during development. The partial copies may also serve as alternative protein-coding units, which allow the pathogen to produce a diverse array of proteins and, consequently, to adapt to its environment.
"Surprisingly, the pi3.4 gene does not code for an effector ?a small protein that elicits a defense response in plants," adds Govers. "Effectors are quite common in fungal and bacterial plant pathogens, including Phytophthora. But in our case, the gene appears to produce a large regulatory protein that exerts its effect by regulating the expression of other genes, possibly effector genes."
While the exact mechanism by which these partial gene copies function as a source of modular diversity remains to be resolved, this study highlights the importance of genome plasticity in evolution. Understanding genome plasticity as a mechanism for environmental response and ecological adaptation in pathogenic organisms has important implications. "The efforts of plan t breeders to obtain resistant varieties by introducing R genes, either by classical breeding or by genetic modification, may be a waste of time and resources when the genome dynamics of the pathogen population is not understood," says Govers. "Monitoring field populations of plant pathogens at the genome level will be instrumental for predicting the durability of R genes in crop plants."