Probing mechanisms of defense gene activation to elevate plant disease resistance.

Intracellular immune receptors in plants are main molecular surveillance mediators in disease resistance, and they are also known as Resistance (R) proteins, nucleotide-binding (NB) and leucine-rich-repeat (LRR) domain-containing receptors (NLRs) and they can form inflammasome-like high-order protein complexes or known as “resistosomes”. Recognition of effectors (molecules secreted by pathogens, and some can suppress the host immunity) leads to the activation of NLR proteins or resistosomes and enhanced disease resistance (also known as effector-triggered immunity, or ETI). An early physiological signature of such activation is the rapid upregulation of defense genes. Malfunction of transcriptional reprogramming in ETI compromises the NLR-mediated immunity.

Recently the Ding Lab has generated multiple novel toolkits to uncouple the general regulatory mechanisms by which defense genes are transcriptionally activated.  We aim to identify and characterize the common regulatory components downstream of NLRs. On one hand, we will focus on understanding the functions of known several transcriptional regulators by answering the following questions: how are they recruited and activated? do they have co-regulators? how do they regulate their downstream targets? One the other hand, we will use novel genetic approaches to uncover novel components that are involved in the activation of ETI.

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