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Refining Defense Gene Activation Mechanisms to Enhance Plant Disease Resistance


Our research revolves around the pivotal role of Intracellular immune receptors in plants as key molecular surveillance mediators in disease resistance. These receptors, also referred to as Resistance (R) proteins, nucleotide-binding (NB) leucine-rich-repeat (LRR) receptors (NLRs), exhibit the ability to form inflammasome-like high-order protein complexes called “resistosomes”. When these receptors recognize effectors, which are molecules secreted by pathogens, some of which can suppress host immunity, it triggers the activation of NLR proteins or resistosomes, resulting in enhanced disease resistance known as effector-triggered immunity (ETI). One of the early physiological indicators of such activation is the rapid upregulation of defense genes. However, dysfunction in the transcriptional reprogramming during ETI can compromise NLR-mediated immunity.

The Ding Lab has recently developed innovative toolkits aimed at unraveling the general regulatory mechanisms that govern the transcriptionally activation of defense genes. Our primary objective is to identify and characterize the common regulatory components downstream of NLRs. On one hand, we are dedicated to gaining a deeper understanding of the functions of several known transcriptional regulators by addressing important questions such as how they are recruited and activated, whether they have co-regulators, and how they precisely regulate their downstream targets. One the other hand, we employ novel genetic approaches to uncover previously unidentified components involved in the activation of ETI.

By leveraging these cutting-edge techniques, our lab strives to shed light on the intricate network of intracellular immune receptors and their associated regulatory pathways. Our ultimate aim is to contribute to the development of innovative strategies for enhancing disease resistance in plants, thereby promoting sustainable agriculture and ensuring global food security.


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