A non-reciprocal translocation prevents effector-triggered immunity

Background

The genomes of microbial pathogens, such as bacteria and filamentous fungi, typically contain genes that encode secreted proteins that assist the pathogen to successfully infect their host by inferring with the host’s immune defenses. These proteins are referred to as effectors. These effectors can be recognized by the host, triggering immune responses. Thus, effectors can be double-edged swords. One of the first studied effectors from a fungus was the Avr9 from the tomato pathogen Cladosporium fulvum. Even though the existence of this effector is known since the late 1980s, its function remains unknown. What was known since then is that strains of C. fulvum that lost the gene encoding Avr9 avoid immune responses in tomato accessions carrying the gene Cf-9, which encodes a receptor protein that recognize Avr9, triggering immune responses.

However, an unanswered question question was:

How strains of C. fulvum lose the gene encoding the effector Avr9?

Major findings

I found out that in the C. fulvum strain Race 2 4 9 11 lost Avr9 due to a non-reciprocal translocation between chromosomes 2 and 7. In simple words, the region of the genome that contained Avr9 was replaced by a different DNA sequence. This DNA sequence that replaced the Avr9 locus is a duplication of a regions from a different chromosome. This one example of a chromosomal structural variation in the genome of a pathogen that prevents effector-triggered immunity.

How did this translocation happened?

The mechanism that could have acted to induce this translocation is unknown. However, I believe that the proximity to the end of the chromosome (subtelomeric region) could have played a role, because these regions are known to frequently harbor mutations. More importantly, I found truncated copies of a tranposable element flanking the border of the translocation. This observation led me to speculate that these truncated copies, which are 95% identical, served as substrate for non-allelic homologous recombination between non-homologous chromosomes.

A manuscript describing this and other findings is currently in preparation.