Abstract
The importance of segmental duplications and copy number variants as a source of genetic and phenotypic variation is gaining greater appreciation, in a variety of organisms. Now, we have identified the Phytophthora sojae avirulence genes Avr1a and Avr3a and demonstrate how each of these Avr genes display copy number variation in different strains of P. sojae. The Avr1a locus is a tandem array of four near-identical copies of a 5.2 kb DNA segment. Two copies encoding Avr1a are deleted in some P. sojae strains, causing changes in virulence. In other P. sojae strains, differences in transcription of Avr1a result in gain of virulence. For Avr3a, there are four copies or one copy of this gene, depending on the P. sojae strain. In P. sojae strains with multiple copies of Avr3a, this gene occurs within a 10.8 kb segmental duplication that includes four other genes. Transcriptional differences of the Avr3a gene among P. sojae strains cause changes in virulence. To determine the extent of duplication within the superfamily of secreted proteins that includes Avr1a and Avr3a, predicted RXLR effector genes from the P. sojae and the P. ramorum genomes were compared by counting trace file matches from whole genome shotgun sequences. The results indicate that multiple, near-identical copies of RXLR effector genes are prevalent in oomycete genomes. We propose that multiple copies of particular RXLR effectors may contribute to pathogen fitness. However, recognition of these effectors by plant immune systems results in selection for pathogen strains with deleted or transcriptionally silenced gene copies.
Highlights
Plant immunity relies on surveillance systems to detect particular infection-specific molecules or perturbations [1,2]
We examine the entire family of predicted RXLR effectors from P. sojae and P. ramorum and provide evidence that multiple, nearidentical copies of particular effectors pervade the genomes of these two species
Further examination of the Avh72 sequence revealed that it encodes a pseudogene because the open reading frame (ORF) is interrupted by a premature stop codon
Summary
Plant immunity relies on surveillance systems to detect particular infection-specific molecules or perturbations [1,2]. Plant pathogens evolve to evade recognition and to suppress plant defenses in order to enhance their fitness and reproductive success. Plant pathogens secrete effector molecules that interfere with plant immune systems or otherwise foster disease [3]. Pathogen effector molecules may come under scrutiny by plant surveillance systems and trigger immunity. This process is called effector triggered immunity (ETI). ETI is a dynamic process that can determine whether disease occurs or not. The genetic components that play a role in this process represent the leading edge in evolution and adaptation in the interaction between the two species, host and pathogen
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