Tandem-repeat modules in phytopathogenic effectors driver their evolution and diversification

Abstract Plant pathogens deliver effector proteins into both the host apoplast and host cells. These effectors function to colonize the host typically by altering host physiology or by subverting plant immune responses. The host plants have evolved intracellular nucleotide-binding site leucine-rich repeat (NBS-LRR) immunoreceptors that directly or indirectly recognize specific effector(s) to trigger plant immunity that prevents colonization. To circumvent effector-triggered immunity, adapted pathogens rely on constantly effectors evolution to further enhance susceptible host colonization. During the past few years, evidence has arisen that many effectors containing tandem repeat modules are particularly prone to rapid evolution through module insertion/deletion/shuffling, point mutations or adoption of other function domains. In this review, we highlight the diverse function of two modular effectors: TAL effectors in prokaryotic bacteria, (L) WY effectors in eukaryotic oomycetes, focus on new insights and the potential role of modularity in effector evolution, and discuss avenues for future research.