Institute for Integrative Genome Biology

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Katherine Borkovich

Professor;
Plant Pathologist;
Fungal Cell Biologist/Biochemist

Mailing Address:

Plant Pathology and Microbiology
Boyce Hall /3453
University of California
Riverside, CA 92521

Phone: (951) 827-2753
Fax: (951) 827-4294
Email: katherine.borkovich@ucr.edu
Website

Degree(s):

PhD 1985 University of California, Los Angeles
BS 1979 University of California, Davis

Center/Inst Affiliation(s):

Center for Plant Cell Biology
Center for Research in Intelligent Systems (CRIS)

Areas Of Expertise:

Environmental Sensing and Signal Transduction in Fungi; Fungal Genetics; High-throughput Genomics; Heterotrimeric G proteins; Two-component Regulatory Systems

Awards / Honors:

2006  AAAS Fellow (American Association for the Advancement of Science)
2001  Dean's Award for Teaching Excellence, U.T.-Houston Medical School
1995, 1999, 2000  Dean's Award for Excellence, U.T.-Houston Graduate School of Biomedical Sciences
1994-97  American Cancer Society Junior Faculty Research Award
1986-89  Postdoctoral National Research Service Award (NIH)
1981-84  Genetics and Regulatory Mechanisms Pre-doctoral Training Grant (NIH)
1980  Outstanding Teaching Assistant Award, Chemistry Department, UCLA
1979  B.S. With Highest Honors, U.C. Davis
1979  Phi Kappa Phi, U.C. Davis Chapter
1976  Edward Frank Kraft Prize for Outstanding Scholastic Record, U.C. Davis

Research Summary:

Genome-Wide Analysis of Neurospora:  Neurospora crassa is a filamentous fungus that is a model for both animal and plant pathogens.  Neurospora has also been designated as a model organism by the National Institutes of Health.  I was heavily involved in the effort to sequence the genome of Neurospora and made numerous contributions to organizing the first community annotation projects.  I am currently Co-PI of a NIH Program Project grant for functional genomics, transcriptional profiling, EST sequencing and manual annotation of the Neurospora genome. My laboratory is involved in the genome-wide targeted gene replacement project, with the goal of mutating all of the more than 10,000 ORFs in Neurospora. We have created the recipient strains, significantly improved the mutation protocol and established a laboratory information management system (LIMS) for tracking samples. We created thousands of mutants that have been sent to a central stock center for distribution to the scientific community. A manuscript summarizing our analysis of 103 transcription factor mutants was published in 2006 in the Proceedings of the National Academy of Sciences, USA.

Heterotrimeric G Proteins in Filamentous Fungi:  In eukaryotic organisms, major signal transduction pathways utilize heterotrimeric (αβγ) G proteins (G proteins). G proteins are involved in numerous processes in mammals, including vision, taste, smell, cardiac function and neurotransmission.  G protein activation involves ligand binding by a seven transmembrane helix G protein-coupled receptor (GPCR), GDP/GTP exchange on the Gα subunit and dissociation of the heterotrimer, freeing Gα and Gβγ to regulate downstream effectors.
    My laboratory discovered G proteins in filamentous fungi.  Later work showed that G proteins are essential for pathogenesis in animal and plant pathogenic fungi.  We have demonstrated that Neurospora G proteins control cell proliferation, asexual and sexual development and stress tolerance. We have recently turned our attention to the approximately 25 predicted GPCRs in the Neurospora genome sequence. Mutational analysis indicates that GPCRs regulate pheromone-dependent chemotropic growth of female hyphae towards male cells, the morphology of fertilized reproductive structures and carbon sensing.
    Our work has revealed common regulatory mechanisms that control regulation of growth and development in Neurospora and pathogenic species. Knowledge of the molecular details of early events in pathogenesis will allow development of new control practices and/or chemical agents to combat fungal diseases in both plants and animals.

Two-Component Regulatory Systems:  Two-component regulatory systems, consisting of proteins containing histidine kinase and/or response regulator domains, regulate signal transduction in bacteria, Archaea, slime molds, fungi and plants. These cascades regulate a diverse array of functions, ranging from responses to nutritional, stress or chemical signals to multicellular development, chemotaxis and light sensing. The genome sequence of Neurospora predicts 11 hybrid histidine kinase, one histidine phosphotransfer protein (HPT) and two response regulator genes. The number of histidine kinase genes is striking, in that the sequenced yeast genomes contain only 1-3 histidine kinase genes. My laboratory has shown that one two-component system is required for osmotic and fungicide resistance, female fertility and proper functioning of the circadian rhythm, through phosphorylation of a downstream Mitogen-Activated Protein Kinase signaling pathway. Analysis of mutants lacking the 11 hybrid histidine kinases is underway.

Chemical Genetics:  I am a participant in the UCR NSF ChemGen IGERT training grant that is focused on screens to identify chemicals that affect the biology of plants and plant pathogens. Mr. James Kim, an IGERT student in my group, is currently screening two different chemical libraries for effects on 1) spore germination and 2) inappropriate asexual spore formation in Neurospora G protein mutants. These screens are extremely relevant, as asexual spores are the primary means by which pathogenic fungi are disseminated in the environment. Furthermore, strains lacking the Gα subunits gna-1 and gna-3 exhibit a profound growth defect, and some of our G protein mutants sporulate inappropriately in liquid culture. Thus, we can use our existing mutants to determine patterns of sensitivity to particular chemicals and gain clues to the overall mechanism of their action. Identification of chemicals that block spore formation and/or germination would provide candidates for fungicides and antifungal drugs.

Selected Publications:

Lab Personnel: +

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