Nian Wang was born in Qufu, in Shandong Province, China. He received his BS degree in Plant Protection from Shandong Agricultural University in 1995 and his MS degree in Plant Pathology from China Agricultural University in 2001. He received his Ph.D. degree in Plant Pathology in 2005 from Texas A&M University under the guidance of Prof. Dennis Gross where he studied the regulation of genes encoding lipodepsipeptide phytotoxins including syringomycin produced by Pseudomonas syringae. His thesis work resulted in several publications in high-impact journals such as MPMI and Journal of Bacteriology. In the fall of 2005, he joined the lab of Prof. Steven Lindow at the University of California, Berkeley as a Postdoctoral Scholar where he performed global transcriptional analysis of the important plant pathogenic bacterium Xylella fastidiosa. This work focused on the regulon under the control of a small signal molecule (DSF) that is central to the regulation of virulence factors in this pathogen. While mutational analyses had revealed that DSF played an important role in regulating virulence of X. fastidiosa, there was little understanding of what constituted virulence factors in this vascular pathogen. The transcriptional analyses preformed by Dr. Wang provided unprecedented insight into what constitutes virulence genes. This work, recently submitted for publication, provided evidence that extracellular enzymes such as polygalacturonaes and type IV pili which had been shown to contribute to virulence were actually suppressed by DSF-mediated signaling, while a variety of adhesins and type I pili were induced in cells as they reached high cell density. Along with many other such regulated genes, his work led to the development of a “biphasic lifestyle” model of X. fastidiosa virulence, in which traits that contribute to plant colonization are expressed only at low cell densities while those involved in insect transmission were expressed in a subset of the cells in plants and only as cells reached high cell densities. This revolutionized our insights into the behavior of X. fastidiosa and suggested new strategies of disease control. In 2007, he was appointed as an Assistant professor in the Department of Microbiology and Cell Science of the University of Florida and is stationed at the Citrus Research and Education center in Lake Alfred where he has initiated a very innovative and productive research program on the study of Huanglongbing disease of citrus (Citrus Greening) as well as Citrus canker caused by Xanthomonas axonopodis pv. citri. In the short 3 years that he has been in his current position, he has already established himself as one of the leaders in the study of citrus greening.
Dr. Wang’s work has provided great insight into the process by which Candidatus Liberibacter asiaticus, the causal agent of Citrus Greening, colonizes Citrus species. Dr. Wang has published seminal work on the detection of Ca. L. asiaticus in citrus and his studies of its distribution and population size in various tissues in infected citrus trees has provided great insight into the infection and disease process. His work using ethidium monoazide (to prevent amplification of DNA in dead bacterial cells) coupled with quantitative PCR has shown that the environment within even susceptible Citrus species is apparently hostile to this pathogen since as many as 80% of all the cells in the plant are dead. His detailed quantitative studies of the population size of Ca. L. asiaticus in different parts of citrus trees differing in disease severity has provided for the first time evidence that a clear threshold population size of this endophytic pathogen must be established before symptoms can occur. His use of such a live/dead PCR assay is a first in plant pathology research, and demonstrates it as a valuable tool to study plant-microbe interactions. Using very powerful new tools to describe both the culturable and unculturable bacterial community within the phloem of citrus trees, Dr. Wang has now shown that there is a surprisingly diverse bacterial community associated with both healthy and diseased trees. More importantly, this work has shown that there is no apparent cooperativity between different bacterial species to initiate disease symptoms in citrus, and thus that infection with Ca. L. asiaticus is sufficient to account for HLB disease. Interestingly, he found some evidence of negative associations between various bacterial taxa and Ca. L. asiaticus, suggesting that antagonism may play an important role in some cases to suppress disease.
Dr. Wang has described the many important changes in plant gene expression that are associated with infection with Ca. L. asiaticus. His work on transcriptional profiling of infected vs. healthy citrus tissues is the first to describe the changes in plant gene expression associated with this disease. Not only was he able to show that there are many plant responses associated with infection, but his work has provided strong inferences about the disease process. For example, his results clearly show that the genes encoding several key starch biosynthesis enzymes are strongly up-regulated and are likely contributing to both the accumulation of starch in infected leaves, but also in the decrease in sucrose transport via the phloem to the roots, and hence disruption of root function. Perhaps more importantly, his work shows that several genes including those encoding PP2, proteins that aggregate to form polymers that can block sieve pores in phloem cells, are strongly induced. The consequence of the enhancement of these proteins that regulate pore aperture in sieve cells is to interfere with downward communication between sugar source tissues in the leaves with sink tissues in the roots. While it has long been thought that the presence of cells of Liberibacter themselves were responsible for blockage of sieve elements, Dr. Wang has now nicely demonstrated using various microscopy methods that Liberibacter does not form cellular aggregates within plants that are capable of blockage of sieve elements, and instead that the host response to Liberibacter infection results in sieve pore plugging. These results all greatly clarify our understanding of the infection process and suggest ways that disease symptoms can be alleviated, by blocking inappropriate host responses.
