Roger Wise was born in El Paso, TX, and raised in Birmingham, MI. He earned a B.S. degree in physiology with high honor from Michigan State University in 1976 and a Ph.D. in genetics from the same institution in 1983, where he investigated the genetics of barley-powdery mildew interactions with Albert Ellingboe. As a post-doc from 1984 to 1986 at the University of Florida with Daryl Pring, he cloned and demonstrated that the novel T-urf13 mitochondrial gene from T-cytoplasm maize caused male sterility and toxin sensitivity and, thus, was the molecular basis for the southern corn leaf blight epidemic of 1970. This was a milestone discovery: T-urf13 was the first cloned plant gene whose product is a target of a pathogen virulence determinant. During a subsequent fellowship at the Max-Planck-Institute, Wise laid the groundwork for his research as a USDA-ARS research geneticist and professor of plant pathology at Iowa State University, a position he assumed in 1989.
Wise has been a leader in applying cutting-edge genetic and genomic approaches to answering fundamental questions in cereal crop disease defense. His early studies identified the first crown-rust resistance (R) gene cluster in oats and were among the first to separate gene-specific resistance from programmed cell death in plants. Featured on the cover of MPMI (2001), these studies were critical to understanding the genetic organization of crown rust resistance. Looking to the future, he subsequently developed barley and powdery mildew as a model gene-for-gene system for cereals and biotrophic pathogens. Wise’s team cloned the Mla R gene via map-based methods, resulting in the first functional analysis of a coiled-coil, nucleotide binding, leucine-rich repeat R protein in the Triticeae. His group first demonstrated R-gene specific transcript induction and the regulation of host-resistance proteins by upstream open reading frames, as well as identifying the single aspartate residue differentiating RAR1-dependent and RAR1-independent MLA proteins. Highlighted on the Plant Journal cover (2004), these findings promoted our understanding of how signals are transmitted to activate defense.
Recent studies in nonhost resistance, as well as host susceptibility, indicate that genes other than those governed by R-AVR interactions also play key roles. Wise conceived and co-led 10 U.S. and international institutions to develop the Barley1 GeneChip, a uniform transcript profiling platform to investigate 22,000 genes simultaneously. He used Barley1 in concert with an elegant experimental design to identify a highly coregulated cluster of 160 basal-defense related genes that were significantly up-regulated in both incompatible and compatible interactions, coinciding with germination of Blumeria graminis conidia and formation of appressoria. Suppression of these transcripts occurs during establishment of the perihaustorial interface only in compatible interactions, whereas these transcripts are sustained or increased in incompatible interactions. This unique regulation of PAMP-triggered, innate immunity provided one of the first genome-wide demonstrations of a link between basal defense and R-gene mediated resistance, shaping current theories of how plants withstand disease. Additionally, the Barley1 project provided the model for other community-based crop and crop pathogen GeneChips, including wheat, corn, rice, Fusarium, grape, and soybean, accelerating molecular plant pathology and crop genome research worldwide.
As a result of these comprehensive gene expression investigations, Wise’s team discovered the novel blufensin family of cereal-specific peptides, and demonstrated that Blufensin1 is a negative regulator of plant defense. Further investigations identified genes involved in nuclear import and the secretory pathway as being regulated by Blufensin1, plant processes that are critical to the genetic brigade that is activated when fungal pathogens establish haustoria in the host. He also recently demonstrated that Ribosomal RNA-processing protein 46, which encodes a critical component of the exosome core, functions as a negative regulator of rRNA processing in R-gene-independent cell death, and that several previously uncharacterized WRKY transcription factors, as well as pivotal branchpoints in the shikimate pathway, influence penetration resistance in Mla-mediated, barley-powdery mildew interactions.
To mitigate emerging disease threats, Wise has employed genetical genomics, in which genome-wide expression profiling is performed on entire segregating populations. With this approach, his team discovered a master switch for disease defense that controls the expression of >500 basal defense genes and colocalizes with an Adult Plant Resistance QTL to Ug99 stem rust. Since Ug99 can devastate yields among nearly all wheat and barley varieties grown worldwide, characterization of the master switch, and development of allele-specific markers, will be used to accelerate the integration of adult plant resistance to Ug99.
As parallel expression coordinator for the International Triticeae Mapping Initiative, Wise spearheaded a team of ISU colleagues in Computer Engineering and Statistics to build PLEXdb, a unified public resource for gene expression for plants and plant pathogens (http://plexdb.org/). PLEXdb currently houses >6,800 GeneChip hybridizations from 232 experiments in barley, wheat, rice, maize, soybean, grape, Fusarium, and Arabidopsis. PLEXdb has been used by over 700 academic, government, and corporate scientists from 80 countries in Europe, Asia, North America, and the Pacific Rim.
Wise’s leadership exemplifies his ability to tackle complex problems as well as his commitment to real-world plant pathology and crop improvement. His contributions include not only groundbreaking discoveries that have profound implications for our understanding of plant-fungal interactions, but also enabling community resources that drive advances across and outside the field of plant pathology. He has successfully mentored generations of undergraduate, graduate, and post-doctoral scientists during his 30 years in APS. He established an NSF-funded K-12 teacher program on Gene Expression and Segregation Analysis in Agriculture and Human Health, impacting greater than 100 underrepresented and underserved students each year. As principal investigator or co-principal investigator, he has garnered continuous federal funding totaling more than $17 million, received more than 50 invitations to speak at universities, national, and international symposia, and authored more than 80 publications in high-impact journals. He has transformed the field by catalyzing the adoption of new technologies, and enabled broad access to new data and powerful tools for analysis. Wise’s sustained excellence in research has contributed significantly to our current understanding of why plants become diseased and how they defend themselves against their pathogens. His scientific and community contributions make him a deserving candidate for APS fellow.
