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Moscow

Department of Biological Sciences
biosci@uidaho.edu
phone: (208) 885-6280
fax:(208) 885-7905
Life Sciences South 252
875 Perimeter Drive MS 3051
Moscow, ID 83844-3051

Dr. Patricia Hartzell

Patricia L. Hartzell, Ph.D.


Office: LSS 150
Email: hartzell@uidaho.edu
Mailing Address: University of Idaho
Dept. of Biological Sciences
875 Perimeter MS 3051
Moscow, ID 83844-3051

College of Science
Professor

Campus Locations: Moscow
With UI Since 1994


  • Research/Focus Areas
    • Prokaryotic development
    • mechanism of phase variation and its role in swarming and development
    • signal transduction with emphasis on GTPase regulatory pathways
    • protein interactions
    • novel myosin-like proteins in prokaryotic motility
    • extremeophile microbiology, biochemistry, oxidative stress
    • genetics and molecular biology.
  • Biography
    I became enthralled with microbes and microbiology when I was a student in California.  At the time, I was very involved in environmental issues and learned about microbes that produce methane during anaerobic respiration. After completing my BS, I studied methanogens with Dr. Mah at UCLA, then moved to Illinois to work on the biochemistry of methane production with Dr. Wolfe. It was an exciting time as Wolfe and Woese had just discovered that methanogens were part of a new domain of life called Archaea. For postdoctoral work, I switched to a completely different organism, Myxococcus xanthus, to learn more genetics. For these studies, I went to Stanford University to work with Dr. Dale Kaiser. I accepted a faculty position at UCLA in 1990, but after four years in Los Angeles (and a long-distance marriage), my husband and I decided to look for jobs in the same location. We fell in love with Idaho — the beauty of Moscow and the people at the University. I've been fortunate to work with many talented students who have made significant contributions toward understanding myxobacterial gliding motility, development, and phase variation.   
  • Selected Publications
    • Furusawa, G., Dziewanowska, K, Stone, H, Settles, M. and P. L. Hartzell* 2011 Global analysis of phase variation in Myxococcus xanthus.  Molecular Microbiology 81: 784-804
    •  Fremgen, S., Burke, N., and P. L. Hartzell*  2010 Domains of MglA critical for gliding and development in Myxococcus. BMC Microbiology 10:295-316
    • Patryn, J., Allen, K., Dziewanowska, K., Otto, R. and P. L. Hartzell*  2010 Localization of MglA, an essential motility protein in Myxococcus xanthus.  Cytoskeleton 67:322-37.
    • Youderian, Philip A, and Patricia L. Hartzell* 2007. Triple Mutants Uncover Three Additional Genes Required for Social Motility in Myxococcus xanthus. Genetics 177:557-66
    • Mignot, Tâm, Joshua W. Shaevitz, Patricia Hartzell, and David Zusman*. 2007. Evidence that Focal Adhesion Complexes Power Bacterial Gliding Motility. Science 315:853-6
    • Youderian, Philip A, and Patricia L. Hartzell* 2006. Transposon insertions of Magellan-4 that impair social gliding motility in Myxococcus xanthus. Genetics 172: 103-15
    • Yang, Ruifeng, Sarah Bartle, Rebecca Otto, Angela Stassinopoulos, Matthew Rogers, Lynda Plamann, and Patricia Hartzell* 2004. AglZ is a filament-forming coiled-coil protein required for gliding motility of Myxococcus xanthus.  J. Bacteriol 186: 6168-6178
  • Research Projects
    To survive changing environmental conditions, microbes have evolved complicated regulatory circuits to integrate the myriad signals that provide needed input for adaptation. Some of the most dramatic adaptive responses manifest as marked changes in cell motility and production of distinct morphotypes or quiescent forms.  Myxococcus xanthus is a soil-dwelling, antibiotic-producing, gliding bacterium that survives in nature by preying on microbes and decaying vegetation. When nutrients are exhausted, cells build multicellular fruiting bodies that contain rod-shaped cells that differentiate into quiescent spores.  We use M. xanthus as a model for the two projects described below.
    • Phenotypic (phase) variation.  The term phenotypic variation is used to describe the ability of microbes to alter the expression of various cellular components, such as flagella or surface proteins.  Some pathogens use phase variation as a means to evade host defenses, thus allowing the microbe to survive destruction by the immune system.  Less is known about phase variation in non-pathogens although preliminary evidence suggests that phase variation contributes to survival of cells in the environment. M. xanthus phase varies between a yellow (DKX pigment +), swarm proficient variant and a tan (DKX pigment -), swarm deficient variant.  Yellow variants can phase to tan and vice versa.  Both cell types play critical roles in survival. Using microarray analysis, we showed that genes for production of secondary metabolites, including the yellow pigment, and autolysis are expressed in the yellow phase. In contrast, tan phase cells express serine-threonine kinases, receptor proteins, and oxidative stress proteins. The expression profiles area consistent with the observed phenotypes. During growth, outward swarming yellow cells produce antibacterial and antifungal compounds that likely protect the slower, more stable tan cells. During development, lysis of yellow cells releases the yellow pigment, which stimulates sporogenesis in the tan phase cells. Hence, a novel type of symbiosis exists between yellow and tan variants. Independent student projects involve using molecular and genetic tools to elucidate the mechanism that allows M. xanthus cells to undergo this remarkable reversible switch and to test the hypothesis that the biological interplay between the two cell types has evolved as a mechanism to favor sporulation.
    • The mechanism of gliding movement.  How does a bacterial cell coordinate the activity of two independent molecular motors to glide over different types of surfaces?  We propose that a small Ras-like GTPase encoded by mglA, the only gene common to both gliding motor systems, synchronizes the two systems and regulates the amplitude of each motor depending on the type of gliding surface. To test our hypothesis, we identified and characterized protein partners for MglA and analyzed the GTPase activity of MglA. We discovered that MglA interacts with at least three other proteins – AglZ (a coiled-coil protein), MasK (a tyrosine kinase) and MglB (a GAP-like protein). Analysis of functional MglA-Yfp in actively gliding cells was used to show that MglA associates with the cytoskeleton to generate a dynamic spiral pattern.  This is consistent with the pattern seen for AglZ and AglU, two other proteins known to be essential for motility. Projects for students will be aimed at expanding our knowledge of the protein complexes that are essential for the gliding motors and using fluorescence microscopy to visualize the dynamic motor complexes.
  • Awards and Honors

    • Decade of Excellence Award, INBRE-NIH, 2011
    • Outstanding Research Award, Gamma Sigma Delta, 2003
    • Postdoctoral Fellowship (Stanford University), American Cancer Society, 1987
    • Postdoctoral Fellowship, Jane Coffin Childs, 1987
    • Arm and Hammer Foundation Achievement Rewards for College Scientists (ARCS) Scholarship 1979-80
    • Member, Mortar Board, 1979-80
    • Outstanding Young Women in America, 1979-80
    • Phi Kappa Phi, California State University, 1979-80
"Imagination is more important than knowledge" Albert Einstein

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