June 20, 2025
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Professor Innes was interviewed by MPMI Assistant Features Editor Meenu Singla-Rastogi
Professor Roger Innes, a newly elected member of the U.S. National Academy of Sciences, is a trailblazer in the field of plant-microbe interactions. Currently a distinguished professor at Indiana University Bloomington, Innes has dedicated his career to uncovering the molecular mechanisms behind plant immunity. When Innes received a call from longtime friend and fellow scientist Pam Ronald, he was struck by a wave of disbelief followed by elation. The news? He had been elected to the National Academy of Sciences (NAS), a crowning recognition of a career spent unraveling the mysteries of how plants and microbes interact.
What began as a childhood fascination with wildlife gradually evolved into a passion for molecular biology, thanks in part to influential mentors and early exposure to nature and science. From early work on Rhizobium signaling to groundbreaking discoveries on disease resistance genes in Arabidopsis, his research has shaped the foundational understanding of how plants detect and respond to microbial threats. Over the years, Innes’ work has led to major advancements in the study of nucleotide-binding leucine-rich repeat (NLR) proteins, the guard model of immune signaling and, more recently, the emerging field of extracellular vesicles and RNA in plant defense. His contributions have not only transformed academic inquiry but also hold powerful implications for sustainable agriculture and crop disease resistance.
Innes’ scientific journey is a powerful reminder that science thrives on curiosity, challenge, and the courage to rethink assumptions. His legacy, already profound, is still unfolding and inspiring countless others to push the boundaries of what we already know in the field of molecular plant-microbe interactions. In this interview, Innes reflects on his scientific journey, the mentors and moments that shaped it, the challenges of mentoring diverse minds and kinds, and the evolving landscape of molecular plant-microbe interactions.
Can you briefly share your journey into science and what first sparked your interest in the field of molecular plant-microbe interactions?
My father had a Ph.D. degree in chemistry, and my two older brothers had Ph.D. degrees in chemistry and physics, so a science path seemed somehow expected. But, as a child, I was more interested in nature and being outside than I was in science. I loved watching nature programs on TV such as “Wild Kingdom” and envisioned myself spending my days outside studying wild animals. Thus, I enrolled in a wildlife management major at Humboldt State University in California for my undergraduate degree and began taking various wildlife biology and ecology courses. As part of that degree, I had to take field ecology. This course made me realize that studying ecosystems and wild animals relied mostly on statistics and correlations and did not involve any sort of experimental tests and that fieldwork was not nearly as romantic as the TV shows made out! On the other hand, I was really enjoying my basic chemistry and genetics classes, especially the lab work. Thus, I switched my major to biology and took a new elective course on Molecular Biology, which was a new field at the time and was being taught by a new assistant professor from Stanford named Mike Bowes who had just completed his Ph.D. degree with Nobel Laureate Arthur Kornberg. Kornberg had just written a textbook on DNA polymerase, which we used in the course. This course cemented my decision to pursue a career in molecular biology, but I was still very interested in interactions between organisms, so I sought out a Ph.D. project that would enable me to apply molecular biology approaches to the study of interorganismal interactions. I ended up at the University of Colorado, Boulder, studying the interaction between clover plants and Rhizobium trifolii, which was my entry into the molecular plant-microbe interactions field.
Were there any key mentors or moments that shaped your scientific path early on?
I credit my mother for getting me interested in nature, as she signed me up for Ranger Rick magazine from the National Wildlife Federation when I was 5 years old and nurtured my curiosity about nature. My high school biology teacher was outstanding and was the first person to make me think that a career in biology was a better fit for me than chemistry or physics, which my older brothers had pursued. In college, I had two young professors who were really dynamic and inspiring, one in molecular biology (Mike Bowes, mentioned above) and one in plant systematics (Mike Messler). Ultimately, my career merged these two areas, which was definitely influenced by these two professors.
Your research has had a significant impact on the field of molecular plant-microbe interactions. How would you describe your most influential work(s) to your colleagues?
I like to think that my Ph.D. work, postdoctoral work, and work as a faculty member have each made distinct contributions. As a Ph.D. student, I was one of the first to show that plant roots secrete compounds that induce expression of Rhizobium nodulation genes and contributed to the identification of these compounds as flavones (Flavones Induce Expression of Nodulation Genes in Rhizobium)—my fourth most highly cited primary research paper. As a postdoc, my major contribution was assisting with the development of Arabidopsis as a model system for studying plant-microbe interactions. More specifically, I was one of the first to clone an “avirulence gene” from Pseudomonas syringae (avrRpt2) that could trigger an immune response in Arabidopsis in a genotype-specific manor. This was an important finding as it demonstrated that Arabidopsis followed the “gene-for-gene” model of pathogen recognition previously described in flax by H. H. Flor and opened the door to cloning plant disease-resistance genes. The paper describing this work is my second most highly cited paper (Identification of Pseudomonas syringae Pathogens of Arabidopsis and a Bacterial Locus Determining Avirulence on Both Arabidopsis and Soybean). Upon starting my independent research lab at Indiana University, my priority was to identify and clone disease-resistance genes in Arabidopsis and to use genetics to identify downstream signaling components. This led fairly rapidly to the cloning of RPM1 and my most highly cited paper (Structure of the Arabidopsis RPM1 Gene Enabling Dual Specificity Disease Resistance), while my former postdoctoral lab used avrRpt2 to clone the corresponding resistance gene RPS2, both of which encoded nucleotide-binding leucine-rich repeat (NLR) proteins. These findings, in conjunction with the cloning of the N gene from tobacco by Barbara Baker‘s group, provided the insight that most plant R genes likely encode NLR proteins, which greatly accelerated cloning of disease resistance genes in crop plants and the use of such sequences for marker-assisted breeding.
The cloning of RPM1 also led to an unexpected finding, and an unplanned collaboration, when we discovered that mutations in RPM1 blocked recognition of two different P. syringae avirulence genes, avrB and avrRpm1 (A Disease Resistance Gene in Arabidopsis with Specificity for Two Different Pathogen Avirulence Genes). My lab was pursuing cloning of the R gene that mediated recognition of avrB, while Jeff Dangl’s laboratory was pursuing cloning of the R gene that recognized avrRpm1. I believe it was at a molecular plant-microbe interactions conference that we noticed our genes were mapping to the same region, which led us to test whether mutants that failed to respond to AvrB also failed to respond to AvrRpm1. When they did, we agreed to team up to complete the laborious process of positional cloning of RPM1. The ability of a single R gene to mediate recognition of two sequence-unrelated avirulence genes was unexpected, because Flor’s model predicted that a single plant disease-resistance gene should recognize only one pathogen avirulence gene. This paper told us that recognition was more complex and was our first hint that recognition might be mediated by an indirect mechanism rather than a direct receptor-ligand interaction.
In parallel to cloning RPM1, we also identified and cloned RPS5, which encodes an NLR protein that mediates recognition of the P. syringae effector AvrPphB, a cysteine protease. As part of that effort, we identified multiple Arabidopsis mutants that failed to recognize AvrPphB that did not map to RPS5. We named these loci PBS for AvrPphB Susceptible. These pbs mutants provided the foundation for much of my subsequent career, as it led to the cloning of PBS1, founding member of the receptor-like cytoplasmic kinase (RLCK) family, PBS2 (renamed RAR1, required for NLR stability), and PBS3 (required for SA synthesis). The work on PBS1, in particular, was key to my future, as we subsequently showed that PBS1 was the direct target of AvrPphB and that cleavage of PBS1 activated RPS5, providing strong mechanistic support for the “guard model” of NLR function (my third most highly cited paper; Cleavage of Arabidopsis PBS1 by a Bacterial Type III Effector). This insight led us to test whether we could alter the specificity of RPS5 by altering the cleavage site within PBS1 so that it could be cleaved by proteases from other pathogens. Significantly, this turned out to be true, as we were able to engineer RPS5 to recognize turnip mosaic virus (TuMV) simply by replacing three amino acids in PBS1 to enable it to be cleaved by the TuMV NIa protease, thus conferring resistance to TuMV (Using Decoys to Expand the Recognition Specificity of a Plant Disease Resistance Protein). This discovery has major translational applications, as it enables us to engineer novel disease-resistance traits in crop plants, which we are currently pursuing in soybean and wheat.
Most recently, we have been pursuing a very different line of research that focuses on the molecular and cellular mechanisms underlying host-induced gene silencing (HIGS). This work arose out of an interest in extracellular vesicles (EVs), which we had observed by electron microscopy when analyzing how plant cells die during a hypersensitive disease-resistance response. The apparent increase in EVs made us wonder how EVs contribute to disease resistance. Reading of the mammalian literature led us to hypothesize that they might function to shuttle small RNAs from plant cells to pathogens. Thus, we set out to purify EVs and characterize their protein and RNA contents. We were one of the first labs to accomplish this (Extracellular Vesicles Isolated from the Leaf Apoplast Carry Stress-Response Proteins). This paper is on track to become the most highly cited paper of my career, as it provides the foundation for a new subfield of molecular plant-microbe interactions research.
Looking back, were there any surprising turns or discoveries in your research that changed your trajectory?
Over the course of my career, I have had many incorrect hypotheses, and the process of disproving these hypotheses has invariably led to much more interesting science. The first was that a single plant R gene-mediated recognition of a single pathogen avr gene. Our discovery that RPM1 mediates recognition of both AvrB and AvrRpm1 was pivotal to us investigating the underlying molecular mechanisms by which NLR proteins are activated and our focus on the guard model. A second one was that plant cells die via fusion of the tonoplast membrane with the plasma membrane during the HR. It was our EM work testing this hypothesis that led to our interest in EVs. We failed to find evidence of PM-tonoplast fusion events but got very excited about EVs, leading to a whole new direction for the lab. Most recently, we have disproved our hypothesis that EVs mediate HIGS. Instead, we discovered that plants secrete naked RNA and RNA-protein complexes independent of EVs. This discovery has led to a new focus on extracellular RNA. Most intriguing, we have just shown that plants secrete RNA onto their leaf surfaces, which is where we now believe HIGS is initiated. We definitely did not expect this when we started our work on EVs.
What does being elected to the NAS mean to you personally and professionally?
It is deeply satisfying as it represents formal recognition by my peers that my lab’s research has had a major impact on the field of plant molecular biology. Peer recognition is fundamental to the scientific process and, ultimately, to feeling your work is important. On a professional level, I am hoping it gives my signature a bit more weight, especially when writing to my congressional representatives about support for science!
What responsibilities do you feel come with this kind of recognition from your peers?
The NAS was founded in1863 by an act of Congress and signed by President Abraham Lincoln as a private, nongovernmental institution to advise the nation on issues related to science and technology. Although the present administration does not appear to be very open to advice from scientists, I feel a strong responsibility to leverage my new status as an NAS member to lobby on behalf of all scientists for evidence-based decision making by our representatives.
What is the biggest challenge you have faced in your research to date, and how did you overcome it?
The biggest challenges come with mentoring individual lab members and helping them overcome their own challenges to ultimately be successful in their careers. Every lab member has their own strengths, weaknesses, aspirations, and challenges. Building on their strengths while minimizing weaknesses and challenges is one of the most important things I must do as a mentor. Addressing this challenge involves a heavy dose of empathy and the ability to listen, along with being a genuine cheerleader for progress.
What advice would you give to early-career scientists hoping to make a lasting impact in the field of molecular plant-microbe interactions?
Focus on what the major (most interesting) unanswered questions are in your topic area and give thought to why these questions remain unanswered. Is there a technical barrier to answering the question? If so, are there new technologies coming along that will enable you to overcome that barrier? If so, learn that technology. Stay on the cutting edge. Even better, help develop the new technology and be the first to apply it to an interesting question.
What do you wish more people understood about molecular plant-microbe interactions research?
The first is that the general public needs to understand that plants get sick too and that healthy plants are central to our current food system. Second, they need to understand that current agricultural practices are not sustainable for the planet in the long term and that we need to reduce our reliance on chemical inputs (fertilizers and pesticides) to make it sustainable. Doing so requires research in molecular plant-microbe interactions.
Are there any emerging areas in your field of research that you think are particularly promising or underexplored?
I am very biased, of course, but I am very excited about our new work on extracellular RNA. We hypothesize that exRNA plays a central role in constructing the plant microbiome. If so, it will bring my research career full circle, as I started out looking at the role of plant root exudates on Rhizobium gene expression during my Ph.D. work. In a related area, I think the new technologies emerging around spatial transcriptomics are very exciting, as they will enable a much deeper understanding of how plant cells and microbes interact down to the single-cell level.
How do you hope your legacy will influence the next generation of scientists?
It brings me great pleasure and satisfaction to see my former students and postdocs having success in their own careers, which have been diverse, from working in biotech companies to federal agencies to academics. I like to think that some of what they learned in my lab with regard to asking and answering scientific questions, and with regard to collaborating with others, is benefiting them in their current pursuits. It also brings me satisfaction to see many other labs delving deeply into the topics that we first pioneered in my group, leading to rapid progress in the molecular plant-microbe interactions field. I expect the number of labs investigating leaf-surface RNA will rapidly expand now that we have published our fist paper on that topic.
