Speaker Biography

Joseph Heitman, MD, PhD

Joseph Heitman, MD, PhD, is a James B. Duke Professor in the Department of Molecular Genetics and Microbiology at Duke University, and serves as director of the Center for Microbial Pathogenesis and the University Program in Genetics and Genomics. His research focuses on the evolution of sex in fungi and the roles of sexual reproduction in microbial pathogens, how cells sense and respond to nutrients and the environment, the targets and mechanisms of action of immunosuppressive and antimicrobial drugs, and the genetic and molecular basis of microbial pathogenesis and development. He received the Burroughs-Wellcome Scholar Award in Molecular Pathogenic Mycology and the AMGEN and Squibb awards for significant contributions using molecular biology to understand human disease and infectious diseases. He is a member of the American Society for Clinical Investigation, and a fellow of the Infectious Diseases Society of America, the American Academy of Microbiology, the Association of American Physicians, and the American Association for the Advancement of Science. Since 1998 he has served as an instructor in residence at the Marine Biological Laboratory Molecular Mycology Course, Woods Hole, MA, and he is a member of the advisory committee for the Fungal Genome Initiative of the Broad Institute. He is an editor of the journals PLoS Pathogens, Eukaryotic Cell, Fungal Genetics and Biology, and Current Genetics, serves on the editorial boards for PLoS Biology, Current Biology, and Cell Host & Microbe, and has edited three textbooks on fungal pathogenesis and genetics. Dr. Heitman received undergraduate and master’s degrees with general and special honors from the University of Chicago. He received medical and doctoral degrees from the Medical Scientist Training Program of Cornell University Medical College and the Rockefeller University, and was an EMBO long-term post-doctoral fellow at the Biocenter in Basel, Switzerland.

Abstract: Microbial pathogens in the fungal kingdom

J. Heitman, Duke University, USA

The fungal kingdom is vast, spanning ~1.5 million species diverse as unicellular yeasts, filamentous fungi, mushrooms, lichens, and both plant and animal pathogens. The fungi are closely aligned with animals in one of eight groups of eukaryotes, the opisthokonts. The two groups last shared a common ancestor ~1 billion years ago, more recently than other groups of eukaryotes. As a consequence of their close evolutionary history and shared cellular machinery with metazoans, fungi are exceptional models for mammalian biology, but prove more difficult to treat in infected animals. The last common ancestor to the fungal/metazoan lineages is thought to have been unicellular, aquatic, and motile with a posterior flagellum, and certain extant species closely resemble this hypothesized ancestor. Species within the fungal kingdom were traditionally assigned to four phyla, including the basal fungi (chytridiomycetes, zygomycetes) and the more recently derived monophyletic lineage, the dikarya (ascomycetes, basidiomycetes). The fungal tree of life project has revealed the basal lineages are polyphyletic, and thus as many as eight fungal phyla. Fungi that infect vertebrates are found in all of the major lineages, and virulence arose multiple times independently. A sobering recent development involves the species Batrachochytrium dendrobatidis from the basal fungal kingdom phylum, the chytridiomycetes, which has emerged to cause global amphibian declines and extinctions. Genomics is revolutionizing our view of the fungal kingdom, and genome sequences for zygomycete pathogens (Rhizopus, Mucor), skin-associated fungi (dermatophytes, Malassezia), and the Candida pathogenic species clade promise to provide insights into the origins of virulence. We will survey the diversity of fungal pathogens, and illustrate key principles revealed by genomics involving sexual reproduction and sex determination, loss of conserved pathways in derived fungal lineages that are retained in basal fungi, and shared and divergent virulence strategies of successful human pathogens, including dimorphic and trimorphic transitions in form.