Pto evolved from malectin-like RLKs phosphorylates AvrPtoB to promote Prf-mediated immunity in Solanum pimpinellifolium
Bacterial speck, caused by Pseudomonas syringae pv. tomato (Pst), is a devastating disease of tomato that severely limits global tomato productivity. Understanding the molecular mechanisms underlying Pst and tomato is essential for developing disease resistant varieties. Here, we demonstrate that Pto, the first disease-resistance gene conferring recognition of a specific pathogen, phosphorylates…
Bacterial speck, a devastating disease of tomato, is caused by Pseudomonas syringae pv. tomato (Pst). To combat this disease, understanding the molecular mechanisms that allow tomato plants to resist Pst infection is crucial. Researchers have discovered that the Pto gene, the first resistance gene found to recognize a specific pathogen, plays a key role in this process.
Pto phosphorylates the bacterial effector AvrPtoB at the serine 335 site, which triggers the dissociation of the Prf immune complex. This enhances immune signaling and reduces bacterial pathogenicity in the plant.
Evolutionary analyses suggest that the Pto-associated proteins evolved from malectin-like receptor kinases (MLRs) through the loss of the extracellular domain. This evolutionary adaptation has led to two key amino acid substitutions in Pto: Arg158 and Glu258. These substitutions replace the ancestral lysine residues found in MLRs, such as SpHREK1-1, SpHERK1-2, and SpHERK1-3.
These changes stabilize Pto by preventing its degradation mediated by AvrPtoB's E3 ubiquitin ligase activity. By phosphorylating a bacterial effector to trigger enhanced immunity, Pto reveals a novel mechanism of action that has shaped it into a stable resistance protein in Solanum pimpinellifolium.
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