Martin (Marty) B. Dickman was born in Flushing, New York. He received his B.S. degree at the University of Hawaii in Hilo, in 1979, and his MS and PhD degrees at the University of Hawaii at Manoa in 1982 and 1986. He was a postdoctoral fellow at Washington State University in 1987 before joining the University of Nebraska as an Assistant Professor in 1987. In 2003 he was named the Charles Bessey Professor in Plant Pathology. He joined Texas A&M University (TAMU) in 2006 as Professor of Plant Pathology & Microbiology. At TAMU, he holds the title of Christine Richardson Professor of Agriculture, and is the Director of the Institute for Plant Genomics and Biotechnology.
Dr. Dickman is a preeminent scientist specializing in the area of genetics and molecular biology of fungi and fungal-plant interactions. He has made numerous advances in our understanding of how necrotrophic fungi through the activity of their metabolites, colonize plants and how plants, upon recognition of the pathogen trigger a response known as apoptosis, a form of programmed cell death (PCD). Dr. Dickman has garnered national and international recognition for his research contributions and has authored numerous refereed articles, published in the most highly respected scientific journals. In addition, Dr. Dickman is an effective mentor who has nurtured the careers of the next generation of scientific leaders. He has also built the Norman Borlaug Center at Texas A&M University into one of the nation’s leading institutions for modern plant biology.
It was commonly thought that many plant pathogens cause disease by overwhelming the host through the production and release of toxins and degradative enzymes. However, Dr. Dickman’s work upended this paradigm by demonstrating that many plant pathogens employ a far more pernicious strategy to compromise a susceptible host. These pathogens release molecules that activate PCD, which induces premature cell death in the infected plant and thereby benefits the pathogen by releasing nutrients that support its growth and proliferation. Dr. Dickman’s elucidation of PCD in plants represents one of the cornerstones inand the field of contemporary plant pathology.
Traditionally, plant pathologists analyzed interactions between pathogens and their hosts using one- dimensional “cause and effect” models where a particular molecular or biochemical process necessarily gives rise to a specific biological outcome. Dr. Dickman’s work challenged this paradigm by demonstrating the importance of cell context and pathogen lifestyle to understanding the dynamics of the plant pathogen interaction. Using mammalian models of apoptosis, Dr. Dickman demonstrated that the outcome of a given interaction is dependent upon which party seizes control of host cell machinery. Moreover, death, in and of itself, can be beneficial or detrimental to either the plant host or pathogen. For a necrotrophic pathogen, the induction of host cell death is good for the pathogen as nutrients from dead cells are made available. Whereas, host cell death for a biotrophic pathogen (e.g., a virus which requires living cells for growth and reproduction), is a host defense response restricting pathogen growth and spread. Thus, the outcome of a given plant pathogen interaction is predicated on who is in control of the cell death machinery. If the pathogen gets the upper hand, plant disease ensues. However, if the plant controls PCD, disease resistance will prevail.
Dr. Dickman played a leading role in demonstrating that PCD is broadly conserved across phylogenetic kingdoms. His observation that animal genes that negatively regulate PCD cannot only be expressed in plants, but remarkably, retain function in a heritable manner. This finding was completely unexpected. First, inspection of plant genomes did not reveal sequences that encode classic PCD genes. Second, at the time these experiments were initially performed, it was generally held that plants are incapable of apoptosis. Finally, the idea that a single animal gene can regulate analogous biological process in plants like PCD was viewed with skepticism. What became apparent in Dr. Dickman’s later work was that in fact plants do exploit PCD as a key component of their development, immunity and stress responses. While the sequence similarity between plant and animal PCD genes may be insufficient for the identification of genes with related functions, he established there is sufficient conservation at the structural level, which dictates function, to identify homologous genes (i.e., the important parts of the molecule’s “business end”, such as an enzyme active site or a helical structure,were conserved). Using this hypothesis, his group uncovered a gene family (“BAG” genes) in plants that function analogously to the corresponding animal genes.
Besides elucidating PCD as an underlying mechanism that is important for understanding plant disease development, Dr. Dickman demonstrated that plant PCD can be exploited for controlling plant disease and improving food security. He incorporated findings from the analysis of PCD in his laboratory to introduce genes involved in PCD from a roundworm (C. elegans) into agronomically important plants, including banana. His work resulted in banana plants that are resistant to devastating fungal plant pathogens. This finding is particularly important for developing countries (e.g., Uganda) where banana is a staple and there are no effective alternatives for disease control (classical breeding cannot be done as production bananas do not seed). The deployment of “anti-death “genes (e.g., ced-9) are a promising innovative approach for disease control with benefits to sustainable crop production worldwide.
