P-106 - A T3SS effector suppresses the expression of a calmodulin-like gene

In nature, the ability of symbionts, parasites, and pathogens to manipulate host behavior is widely observed, yet the underlying mechanisms remain largely uncharacterized. Xanthomonas euvesicatoria (Xe) is a gram-negative bacteria that causes black spot disease in Solanum lycopersicum (tomato). During pathogen attack, tomato undergoes transcriptional reprogramming to enhance its defenses. In response, Xe has evolved a suite of effector proteins to modulate host immunity, including XopD, a Type 3 effector protein secreted and injected into host cells. Upon relocalization to the nucleus, XopD has been reported to decrease the stability of SlERF4, an ethylene-sensitive transcription factor. More recently, XopD has also been found to act as a transcriptional activator of DH1, a basic Helix-Loop-Helix (bHLH) transcription factor in tomatoes. DH1 is thought to regulate genes involved in plant defense and growth, though its primary target genes remain unidentified. Bioinformatic analysis of RNA-seq data and RT-qPCR has revealed that XopD and DH1 may suppress the expression of SlCML39, a putative calcium sensor. Given the crucial role of calcium signaling in plant defense, lower expression of SlCML39 can be a mechanism that suppresses immunity and enhances virulence. Our ongoing research aims to characterize the function of SlCML39 in growth and defense. This work describes how bacteria manipulate plant-microbe interactions at the molecular level to affect disease phenotypes.