Rosemary Loria was born May 18, 1952, in Detroit, MI. She received her B.S. degree in 1974 from Lyman Briggs College, Michigan State University (MSU) and her M.S. (1977) and Ph.D. (1980) degrees also from MSU. In 1980, Loria became an assistant professor in the Department of Plant Pathology at Cornell University. She was promoted to the rank of associate professor in 1986 and professor in 1996. She was initially stationed at the Long Island Horticultural Research and Extension Center in Riverhead, NY, where she worked on a variety of diseases of potato. In 1988, her research program moved to the Cornell campus in Ithaca. Although she continued to work on silver scurf caused by Helminthosporium solani and other potato diseases, her research focus shifted increasingly to potato scab caused by Streptomyces scabies and a few other Streptomyces spp.
During the past 25 years, experimentally amenable Gram-negative bacteria have become preeminent models in molecular plant pathology, while the equally important but more recalcitrant Gram-positive plant pathogens have received far less attention. Loria’s research on Gram-positive Streptomyces species has played a major role in correcting this imbalance and is providing new tools and a picture of virulence that is as comprehensive and mechanistically detailed as that for any Gram-negative phytopathogen. Her early work on S. scabies and related species focused on taxonomy and population dynamics, but in 1995 she published a paper in Phytopathology describing the production of the known S. scabies phytotoxin thaxtomin A in culture and a tuber slice bioassay for detecting thaxtomins and identifying pathogenic Streptomyces strains. With these tools in hand, Loria began exploring the biosynthesis and mode of action of thaxtomin, the existence of novel virulence factors, and the genetics of virulence in Streptomyces.
Because thaxtomin is a dipeptide (comprised of phenylalanine and a nitrated tryptophan), Loria and her team postulated that its synthesis involved a nonribosomal peptide synthase (NRPS). Following this hunch, they successfully used degenerate oligonucleotide primers corresponding to a conserved NRPS domain to clone the txtA and txtB genes. By mutating txtA and then complementing the mutation, they obtained the first genetic evidence that thaxtomin production plays a critical role in pathogenesis. They then sequenced DNA in the regions flanking txtA and txtB and discovered txtC, encoding a P450 monooxygenase required for post-cyclization hydroxylation of the dipeptide, and a gene encoding a protein with high similarity to mammalian nitric oxide synthases (NOS). Loria's team, including collaborators Donna M. Gibson (USDA/ARS) and Brian R. Crane (Cornell), reported in 2004 in Nature that the Streptomyces NOS is responsible for the nitration of thaxtomin. Having identified most of the genes directing the biosynthesis of thaxtomin, the Loria group is now elucidating the order in which these enzymes work and has recently determined that the nitration occurs before synthesis of the dipeptide, and therefore that 4-nitrotryptophan represents a novel NRPS substrate.
Loria also noted that the ability of thaxtomin to suppress seedling growth, inhibit cytokinesis, and cause plant cell hypertrophy suggested disruption of cell wall biosynthesis. This hypothesis was confirmed through a collaboration with Chris R. Somerville, at Stanford University, which revealed thaxtomin to inhibit 14C-glucose uptake into the cellulosic fraction of Arabidopsis thaliana cell walls. Interestingly, cellotriose is released from rapidly growing plant tissues, and the Loria group discovered that cellotriose induces thaxtomin production in pathogenic Streptomyces species, which is consistent with the susceptibility of these tissues.
Loria and her team also determined that the genetic basis for thaxtomin production is associated with a pathogenicity island that is present in the few Streptomyces species that are plant pathogenic. The horizontal transfer of this pathogenicity island likely underlies the emergence of new pathogenic species, such S. turgidiscabies, and suggests limits on the durability of cultural practices to manage potato scab. The Loria group was able to observe mobilization in the lab of the of the S. turgidiscabies pathogenicity island to the nonpathogen S. diastatochromogenes, and with it the ability to produce thaxtomin and colonize excised potato tuber tissue. The 2005 Molecular Microbiology paper describing this remarkable finding was also the first report of a pathogenicity island in a Gram-positive plant pathogen.
The Loria group has identified additional virulence determinants, all of which appear to be horizontally acquired and are represented in the S. turgidiscabies pathogenicity island that harbors the thaxtomin biosynthesis genes. The first of these to be found was Nec1, a secreted protein that is produced by most scab-causing Streptomyces species (but not by other Gram-positive plant pathogens) and which triggers necrosis in a wide range of plant species. The second novel virulence factor was found when sequencing the S. turgidiscabies pathogenicity island revealed genes homologous to the Rhodococcus fascians plant fasciation (fas) operon, which direct cytokinin biosynthesis and enable this Gram-positive bacterium to cause leafy galls. Remarkably, a thaxtomin-deficient S. turgidiscabies was found to cause leafy gall symptoms in A. thaliana. Another potential virulence factor discovered by DNA sequencing of horizontally acquired genome regions is a secreted saponinase that is predicted to cleave defense-associated plant saponin glycosides that can complex with sterols in eukaryotes. Intriguingly, a homolog of this gene has been studied in another Gram-positive plant pathogen, Clavibacter michiganensis subsp. michiganensis. Thus, Loria’s work with Streptomyces is providing a broader view of virulence mechanisms in Gram-positive plant pathogens in general. Finally, Loria is leading a USDA-funded sequencing project, in collaboration with the Sanger Institute, to sequence the 10,148,695-bp genome of S. scabies. The genome sequence is now complete and available from the Sanger Institute, and annotation and publication are in progress.
Loria has also held a number of administrative positions at Cornell. She served as chair of the College of Agriculture and Life Sciences Faculty Senate from 1997 to 1998. She served for eight months in 1999 as associate director of the Office for Research and of the Cornell University Agricultural Experiment Station and then from 1999 to 2005 as chair of the Department of Plant Pathology at Ithaca. In addition, from 2002 to 2005 she was director of the Northeast Plant Diagnostic Network.
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