This topic is an excellent gene-environment interactions example. Attack of a fungus (environmental signal) on the host (a corn plant) results in genes (responding to the environmental signal) that mobilize a chemical (kiwellin-1) to defend itself against the invading fungus. Organisms, such as fungi, that cause disease in plants, often secrete proteins that aid the fungus’s growth and reproduction in the host. These are termed effector proteins, and some like to manipulate key metabolic pathways in the plant. Authors [see attached article] identified a protein in maize (corn) that blocks the enzymatic activity of a fungal effector enzyme — thereby preventing the effector’s ability to influence maize metabolism in a way that limits the plant’s defense response.
Authors studied infection of maize by the fungus Ustilago maydis, which can cause corn smut disease and results in substantial crop loss worldwide. The enzyme chorismate mutase (Cmu1), which converts chorismate to prephenate, is a known effector protein of this fungus.
Authors engineered a tagged version of Cmu1 to search for any plant proteins that might interact with Cmu1 in maize leaves infected specifically with U. maydis. Authors found a maize protein (which they call ZmKWL1) that binds to Cmu1. They then determined that ZmKWL1 is a member of a family of 20 proteins (in maize) called the kiwellins, and only ZmKWL1 was highly expressed in response to the U. maydis infection. Furthermore, ZmKWL1 exclusively bound and inhibited purified U. maydis Cmu1 in cell culture, whereas maize versions of chorismate mutase were not affected by ZmKWL1 (the specificity of this interaction is remarkable, given the structural similarity between the fungal and maize enzymes).
Phylogenetic analysis suggests that plant kiwellins have a versatile scaffold that can specifically counteract pathogen effectors such as
Cmu1. During colonization, the fungal enzyme Cmu1 is translocated to the cytosol of plant cells, where its chorismate mutase activity seems to channel chorismate into the phenylpropanoid pathway — thereby preventing biosynthesis of salicylic acid, a central signal for plant innate immune responses against biotrophic pathogens. Interfering with salicylic acid biosynthesis pathways is a well-known general strategy of plant-pathogenic fungi, oomycetes (fungus-like filamentous, microscopic, absorptive organisms that reproduce both sexually and asexually) and nematodes (roundworms). Salicylic acid is used by secreted chorismate mutase and isochorismatase enzymes.
Nature 31 Jan 2o19; 565: 650–653 [article] & pp 575-577 [News’N’Views editorial]