Welcome to the Dong Lab website. We are part of the Biology Department at Duke University. We are located on the West campus on Science Drive in the French Family Science Center.
From Dr. Dong:
Since 1992, my laboratory at Duke University has been working on plant-microbe interactions with the focus on the plant defense response known as systemic acquired resistance (SAR), which when induced can provide protection against a broad spectrum of pathogens.
We first performed a reporter-assisted genetic screen and identified several key components in this inducible defense response, including NPR1. Like NF-kB/IkB in the mammalian immune system, NPR1 is a key regulator in plants controlling multiple immune responses including SAR. My lab made many key discoveries in our understanding of NPR1 function. We found that like NF-kB in mammals, NPR1 is nuclear translocated upon induction. In the absence of pathogen challenge, NPR1 is retained in the cytoplasm as an oligomer through redox sensitive intermolecular disulfide bonds. Upon induction, NPR1 monomer is released to enter the nucleus.
Recently, we reported that nitric oxide and thioredoxin are the redox mediators of NPR1 translocation. Discovery of this novel regulatory mechanism provided new insights into how pathogen-induced cellular redox changes lead to induction of immune responses in plants. In the nucleus, NPR1 serves as a cofactor to transcription factors, such as TGAs, in regulating defense-related genes. The transcriptional activity of NPR1 is regulated both positively and negatively by the proteasome. Before induction, NPR1 is degraded in the nucleus to dampen basal gene expression. Whereas after induction, NPR1 is phosphorylated, ubiquitinylated, and degraded to stimulate target gene expression through accelerated recycling of the transcription initiation complex. Our work demonstrates for the first time proteasome-coupled transcriptional regulation plays a regulatory role in SAR. This finding may have a broad impact to plant research as proteasome has been found to play a key role in many plant hormonal signaling pathways.
Besides our pioneering genetic and biochemical work, we have also made several breakthroughs using genomic approaches. Through an innovative microarray technique, we identified ER-resident genes as direct transcriptional targets of NPR1 and established their role in modification and secretion of antimicrobial proteins. This work revealed for the first time the importance of ER function to plant immune responses. Expression studies also led to the discovery of crosstalks between different plant defense and growth hormone signaling pathways. Induction of SAR involves downregulation of the growth hormone auxin signaling. Crosstalk inhibition between salicylic acid and jasmonic acid is spatially controlled.
The most recent success in our genomic study involves the identification of 22 new components in R gene-mediated resistance against downy mildew. This large-scale functional analysis led to the dissection of R gene-mediated resistance into distinct physiological responses and the establishment of molecular basis for this defense mechanism. Recently, we have developed a new research interest in studying the relationship between chromatin stability and plant defense. Genetic screen for SAR-related mutants led to the surprising identification of multiple genes involved in chromatin stability and modification. We are currently pursuing a possible link between SAR, a short-term immune response, with plants long-term survival strategies during evolution.