Johal is a dynamic scientist whose insatiable scientific curiosity has led his research to have many impacts in plant biology and agriculture. His major focus is to investigate how plants cope with stresses imposed by an ever-changing environment. This he pursues in the context of a couple of bona fide diseases of maize, as well as using maize lesion mimic mutants that form disease-like symptoms in the absence of pathogens. Another area of research is gene discovery, especially those genes that have an agronomic potential and which evolved naturally in maize.

Johal's research over the years has established some major landmarks in the area of plant pathology. His graduate research showed that the key reason why Roundup is such an effective heribicide is because it impairs plants' ability to defend against pathogens, and it does so by suppressing the formation of antimicrobials derived through the shikimate pathway inhibited by Roundup. Johal's postdoctoral research resulted in the cloning of a first ever disease resistance gene in plants (Science 258:985), something that was considered a holy grail at that time. Therefore, one impact of this accomplishment was that it led Johal's postdoc mentor, Steve Briggs, to win membership in the National Academy of Sciences. This was the first time that a plant scientist who had never worked in Academia was elected to this academy.

The cloning of this disease resistance gene (called Hm1) also allowed Johal to work out the biochemical mechanism underlying Hm1-conferred resistance. He showed that Hm1 encodes an NADPH dependent reductase, whose function is to inactivate a virulence factor (HC-toxin) produced by Cochliobolus carbonum (CC), a fungal pathogen of maize. Considered as a host specific toxin, HC-toxin is a small cyclic tetrapeptide molecule with an epoxide group, and it converts CC from a benign pathogen of maize to one that is perhaps the most destructive. An additional impact of this research was that it settled a long and bitter dispute among plant pathologists about the concept and significance of host specific toxins in plant disease.

Recent research on this disease has allowed Johal to show that Hm1 is a grass-specific disease resistance gene that evolved in a common ancestor of grasses about some 50 million years ago. It probably happened as an adaptive strategy to contend with CC or CC-like pathogen capable of producing HC-toxin. When Hm1 breaks down, as it happened naturally in maize that led to the discovery of the disease and CC as a pathogen (PNAS 95:1686), or was forced to do so experimentally in barley (PNAS 105:1762), plants of the grass family become susceptible to disease by CC, elevating the Hm1 gene to the status of a guardian of grasses.

Johal is presently elucidating the mode of action of HC-toxin whereby it enables CC to colonize maize. He is also addressing why some other alleles of Hm1 confer protection against CC only during adult stages of the plant, another issue of longstanding interest and curiosity in plant pathology. The picture that is emerging is again going to unfold a new chapter in plant pathology by bringing - for the first time - the carbon/energy status of the host into the realm of immunity against pathogens.

After joining University of Missouri as an Assistant Professor in 1993, Johal turned his attention to the phenomenon of disease lesion mimicry in maize. Although dozens of mutants had been collected in maize which formed disease like symptoms in the absence of infectious agents, nothing was known about what was ailing them. Johal recognized the potential and opportunity that these lesion-mimic (Les) mutants provided to understand how plants cope with ever-present stresses and became a pioneer in characterizing genes and mechanisms that were malfunctioning in these mutants. Johal showed that while some of them had defects in disease resistance genes and pathways, most others were the result of errors and impairments in diverse metabolic pathways, including those involved in the biosynthesis and degradation of chlorophyll (Cell 89:25; Plant Cell 10:1095).

Johal continues to make high impact contributions in this area. While working with the Les mutants, he noticed that the severity of these mutants was easily influenced by the genetic background of the host plant, in that the same mutant would have a lethal phenotype in one genetic background but only a benign one in another. These observations led Johal to conceptualize that the easily visible and quantifiable phenotype of the Les mutants could be used as a reporter or assay to dissect the genetic basis of the age-old question of the 'genetic background' phenomenon. This quest resulted in the identification of a major QTL that suppresses cell damage associated with multiple mutants and stresses in maize. This QTL has been effectively reduced to a single gene and is being cloned in collaboration with Pioneer Hi-Bred. Although Slm1 was identified on the basis of its ability to suppress a lesion mimic mutants, hence its acronym Slm1 (suppressor of lesion mimics), Johal found that it also confers on corn plants an ability to staygreen following reproduction. This characteristic of Slm1 was confirmed in collaboration with Mitch Tuinstra and has become the focus of a collaborative project recently funded by USDA-AFRI, with Mitch as the PI.