( enes says Dr. Francine Govers the pr...)Potato blight pathogenicity explained by genome plasticity

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
'"/>

Source:Cold Spring Harbor Laboratory