Walter Gassmann was born in Karachi, Pakistan. He received his Dipl. Rer. Nat. (M.S.) degree in 1990 from the Swiss Federal Institute of Technology Zurich (ETHZ) and his Ph.D. degree in plant biology from UC San Diego in 1996 researching plant membrane transporters in the lab of Dr. Julian Schroeder. In 2000, he joined the Department of Plant Microbiology and Pathology (now Division of Plant Science and Technology) at the University of Missouri and is currently a professor in the division ,as well as the director of the Bond Life Sciences Center.
Walter is an outstanding researcher and educator and is a caring, thoughtful highly valued colleague who is motivated by a strong sense of community. The quality, creativity, and significance of Walter's research has led to national and international recognition as a leading program in the molecular characterization of the plant defense response to pathogens. As a postdoctoral researcher in the lab of Dr. Brian Staskawicz, UC Berkeley, he cloned and characterized RPS4, genetically specifying resistance in response to the bacterial effector AvrRps4. RPS4 was one of the founding members of the Toll/Interleukin-1 Receptor–Nucleotide Binding Site–Leucine-Rich Repeat (TNL) class of plant innate immune receptors and became a favored model of many groups to dissect TNL signaling, e.g., leading to the demonstration by the Narusaka lab that RPS4 is paired with RRS1 to recognize a range of effectors from bacteria and fungi. His lab at MU, which he started as an assistant professor in the Department of Plant Microbiology and Pathology in 2000, cloned the second antibacterial resistance gene of the same class, RPS6, specifying resistance to HopA1.
Walter's early work at MU focused on the fine-tuned regulation of RPS4 expression and function by alternative splicing of RPS4 transcripts. His lab was able to show that a fully spliced cDNA of RPS4 did not complement a rps4 mutant and, more importantly, showed reconstitution of RPS4 function by expressing a combination of cDNAs encoding the predicted products of regular and alternative transcripts. This reconstitution was one of the first direct demonstrations that alternative splicing has functional significance in plants. Follow-up work also demonstrated that the ratio of regular transcripts encoding full-length RPS4 and alternative transcripts encoding truncated TIR-NBS versions changed during effector-triggered immunity, with alternative transcripts rising from a small percentage at resting state to the majority of RPS4 transcripts for a brief window of time; these truncated versions of RPS4 that arise naturally from the alternative splicing process autoactively induce a hypersensitive response when transiently expressed in tobacco. Progress in the field on linking domains of resistance proteins to activation by TIR domain enzymatic functions and self-inhibition by the LRR domain support the proposition made at the time that this dynamic of RPS4 alternative splicing during effector recognition functions to accelerate the immune response.
The innate immune response triggered by TNL and related immune receptors is very potent at preventing pathogen spread. Consequently, this response also has the potential to be detrimental to the host if not regulated properly. Apart from the regulation of immune receptor expression and accumulation, it is still unclear how this fine-tuning of the immune system is achieved. Walter addressed this gap in knowledge directly with a genetic screen for mutants with a narrowly defined upregulation of immune receptor signaling and isolated SRFR1, a negative regulator of plant immunity. Interestingly, SRFR1 is a pioneer protein widely conserved between plants and other organisms, including humans. To date, Arabidopsis SRFR1 is the only family member with an assigned function. The interaction of SRFR1 interaction with the positive immune regulator EDS1 and TNL resistance proteins is a direct link to the immune system that is likely to keep the system in an off state. This insight also led to the realization that TNL proteins interact with EDS1. Another facet is the interaction of SRFR1 with TCP transcription factors, which were identified as interactors in a yeast two-hybrid screen against a comprehensive Arabidopsis transcription factor library. Interestingly, around the same time TCP transcription factors also were identified as prominent targets of effectors of pathogens from three kingdoms of life. A recent ChIP-Seq study of TCP8, one of the main TCP interactors of SRFR1, in Walter's lab has shown that TCPs can modulate several hormone and stress pathways, which explains why pathogen effectors target them. These insights also have broadened the impact SRFR1 has on nonimmune plant functions, and this aspect is an active research area in the lab.
In recent years, Walter's work also has returned to its beginning, to AvrRps4, a bipartite effector that is processed once it enters the host cell. Much work has focused on the C-terminal domain (AvrRsp4-C) that in elegant work by others has been shown to interact with the integrated WRKY decoy domain of RRS1 that is necessary to trigger the RPS4/RRS1 pair. Subsequent work by Walter's lab has shown that the AvrRps4 C-terminal domain is not sufficient and that the larger N-terminal domain (AvrRps4-N) contributes to RPS4/RRS1-mediated immunity. This effector-like function of AvrRps4-N was supported by his lab's discovery that Lactuca sativa responds to transient expression of AvrRps4-N with a hypersensitive response that is weakened if AvrRps4-C is coexpressed, providing an explanation why evolution retained this fusion of two effector domains. Ongoing work in Walter's lab is geared toward identifying the host protease that processes AvrRps4 and host targets of AvrRps4-N.
Recognition of Walter's expertise has led to numerous invitations to serve on grant panels for the National Science Foundation, USDA-NIFA, and the Agence Nationale de la Recherche, France, as well as the Donald Danforth Plant Science Center Scientific Advisory Board. He currently serves as an associate editor for Frontiers in Plant Pathogen Interactions and Plant Molecular Biology. In his role as director of the Life Sciences Center at MU, he provides leadership for a diverse group of 31 faculty researchers focused on human and animal health, the environment, and agriculture. Walter exemplifies the qualities of sustained excellence and leadership in research in molecular plant pathology.
