On the evolution of decoys in plant immune systems

TL;DR

This paper presents a quantitative model of decoys in plant immunity, analyzing their roles as immune triggers or pathogen sinks, and identifying conditions for their optimal function based on cellular chemistry and infection outcomes.

Contribution

It introduces a proof-of-principle model linking cellular chemistry to decoy functions, providing insights into their evolutionary roles in plant immune responses.

Findings

Decoys can act as immune triggers or pathogen sinks depending on conditions.

Optimal decoy function depends on pathogen effector binding dynamics.

Model identifies conditions favoring decoys as immune activators or suppressors.

Abstract

The Guard-Guardee model for plant immunity describes how resistance proteins (guards) in host cells monitor host target proteins (guardees) that are manipulated by pathogen effector proteins. A recently suggested extension of this model includes decoys, which are duplicated copies of guardee proteins, and which have the sole function to attract the effector and, when modified by the effector, trigger the plant immune response. Here we present a proof-of-principle model for the functioning of decoys in plant immunity, quantitatively developing this experimentally-derived concept. Our model links the basic cellular chemistry to the outcomes of pathogen infection and resulting fitness costs for the host. In particular, the model allows identification of conditions under which it is optimal for decoys to act as triggers for the plant immune response, and of conditions under which it is optimal for decoys to act as sinks that bind the pathogen effectors but do not trigger an immune response.