Taken together, these findings suggest an unusual genomic strategy to support the rapid evolution of critical genes, known as "effector" genes. Effector genes can disrupt plants' normal physiology, enabling the pathogen to establish a foothold. However, some can also trigger plants' immune responses, making them prime targets for combating P. infestans infection.
"We think this could be a tactic that enables P. infestans to rapidly adapt to host plants," said co-lead author Brian Haas, manager of genome annotation, outreach, bioinformatics, and analysis at the Broad Institute. "In contrast to the well-conserved regions where most genes are found, the repeat-rich regions change rapidly over time, acting as a kind of incubator to enable the rapid birth and death of genes that are key to plant infection. As a result, these critical genes may be gained and lost so rapidly that the hosts simply can't keep up."
Importantly, the new P. infestans genome sequence enabled the researchers to identify many previously unknown effector genes, particularly those that belong to two key groups, known as RXLR genes and CRN genes. The research team identified more than 500 RXLR genes and nearly 200 CRN genes, significantly more than are found in the pathogen's relatives.
These findings not only expand the catalog of known P. infestans genes, they also highlight a critical subset of genes undergoing rapid turnover. Further studies of these genes will f
|Contact: Nicole Davis|
Broad Institute of MIT and Harvard