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Nicole Grieshaber

Nicole Grieshaber

Research Assistant Professor

Office

Life Sciences South 164B

Phone

208-885-0001

Mailing Address

Dept. of Biological Sciences
University of Idaho
875 Perimeter MS 3051
Moscow, Idaho 83844-3051

Research: Biomedical Science, Cellular & Molecular Biology

  • PhD, Molecular Biology, University of Wyoming, 2000
  • BS Microbiology, Colorado State University, 1992

Chlamydia is a group of obligate intracellular bacterial pathogens causing a wide variety of diseases in humans and other animals. In order for Chlamydia to successfully establish a productive infection it must complete multiple rounds of differentiation, alternating between the infectious elementary body (EB) cell type and replicative reticulate body (RB) cell type. My research focuses on the molecular mechanisms and pathways that regulate the developmental cycle of Chlamydia.

After earning my B.S. in Microbiology at Colorado State University, I worked both in the biotech industries and then in academia in Denver, Colorado before deciding to pursue a Ph.D. I conducted my graduate work at the University of Wyoming studying follicle stimulating hormone induced cell signaling in a granulosa cell model. Deciding that 7200 ft above sea level and constant wind was not for me, I finished in under four years and moved to beautiful Hamilton, Montana to start my post doctoral studies with Dr. Ted Hackstadt at the RML where I studied the developmental cycle of the obligate intracellular pathogen, Chlamydia. Upon completion of my graduate work, my husband, two small children and I moved to sunny Florida where I continued my work on regulation of the chlamydial development cycle at the University of Florida. I also branched out a little and started work on unraveling the small RNA networks of the dental pathogen, Porphyromonas gingivalis. Eventually the West, four separate seasons and small friendly towns beckoned, and we moved to The University of Idaho in 2014 where my research on the chlamydial developmental cycle continues.

  • Grieshaber N., Tattersall JS., Liguori J., Lipat J., Runac J., Grieshaber S. Identification of the base-pairing requirements for repression of hctA by the small RNA IhtA leads to the discovery of a new mRNA target in Chlamydia trachomatis. (In Revision)
  • Grieshaber S., Grieshaber N. (2014) The role of the chlamydial effector CPAF in the induction of genomic instability. Pathog Dis. 72 (1), 5-6.
  • Phillips P, Progulske-Fox A, Grieshaber S, Grieshaber N. (2013) Expression of Porphyromonas gingivalis small RNA in response to hemin availability identified using microarray and RNA-seqanalysis. FEMS Microbiol Lett. 351(2), 202-208.
  • Tattersall J., Rao, G.V., Runac, J., Hackstadt, T., Grieshaber, S.S., Grieshaber, N.A. (2012) Translation Inhibition of the Developmental Cycle Protein HctA by the Small RNA IhtA is Conserved Across Chlamydia. PLoS ONE 7(10): e47439.
  • Grieshaber SS., Grieshaber N.A., Miller N., Hackstadt T. 2006. Chlamydia trachomatis causes centrosomal defects resulting in chromosomal segregation abnormalities. Traffic. 7(8), 940-9.
  • Grieshaber N.A., Sager JB., Dooley CA., Hayes SF., Hackstadt T. 2006. Regulation of the Chlamydia trachomatis histone H1-like protein Hc2 is IspE dependent and IhtA independent. J. Bacteriol. 188(14), 5289-92.
  • Grieshaber N.A., Grieshaber S.S., Fischer E.R., Hackstadt T. 2006. A small RNA inhibits translation of the histone-like protein Hc1 in Chlamydia trachomatis. Mol Micro. 59(2), 541-50.
  • Grieshaber N.A., Fischer E.R., Mead D.J., Dooley C.A., Hackstadt T. 2004. Chlamydial histone-DNA interactions are disrupted by a metabolite in the methylerythritol phosphate pathway of isoprenoid biosynthesis.  Proc Natl Acad Sci U S A. 101(19):7451-6.
  • Grieshaber S.S., Grieshaber N.A., Hackstadt T. 2003. Chlamydia trachomatis uses host cell dynein to traffic to the microtubule organizing center in a p50 dynamitin independent process. J Cell Sci. 116(Pt 18):3793-802.

Chlamydia

Chlamydia is a group of obligate intracellular bacterial pathogens causing a wide variety of diseases in humans and other animals. In order for Chlamydia to successfully establish a productive infection it must complete multiple rounds of differentiation, alternating between the infectious elementary body (EB) cell type and replicative reticulate body (RB) cell type. My research focuses on the molecular mechanisms and pathways that regulate the developmental cycle of Chlamydia.

  • Nucleoid Structure. The infectious EB cell type is characterized by a tightly condensed nucleoid structure comprised of genome and two chlamydial histone H1 related proteins, HctA and HctB. Upon infection of the host cell the histones are released, the genome relaxes and transcription/translation begins, initiating EB to RB differentiation. New histones are expressed late in the chlamydial cycle leading to re-compaction of the genome, down regulation of gene expression and RB to EB re-differentiation. Histone DNA binding dynamics likely influence gene expression by altering DNA structure, perhaps by binding to specific nucleating sites on the chromosome. The goal of this arm of research is to determine the role of the chlamydial histones in organizing the structure of the chromosome and to identify their role in gene expression control during development.
  • Small regulatory RNAs (sRNAs). sRNAs regulate a variety of bacterial processes, including virulence, quorum sensing and stress response, primarily by binding specific mRNA targets and regulating their expression. We have shown that a sRNA (IhtA) controls major changes in the life cycle of C. trachomatis associated with pathogenicity. We have additionally identified multiple sRNAs expressed by Chlamydia over the developmental cycle. The goal of this area of research is to identify the mRNA targets of these sRNAs and determine their role in differentiation.

Porphyromonas gingivalis

Porphyromonas gingivalis (Pg) is a pathogen of adult periodontitis and is implicated in multiple systemic inflammatory conditions including cardiovascular disease. Pg‘s ability to invade a wide variety of host cell types and employ adaptive mechanisms to subvert specific host responses are key virulence factors critical to its survival and persistence.

sRNA regulation of gene expression is key to rapidly responding to changing environment. We have previously identified a number of sRNAs regulated by various virulence conditions. Unfortunately, techniques to identify the mRNA targets of sRNAs are quite limited. Along with a collaborator at the University of Florida, we are developing a novel unbiased screening model using an E. coli surrogate host, capable of identifying both positively and negatively regulated mRNA targets.

  • NIH Fellows Award for Research Excellence, 2002
  • NIH Intramural Research Training Award, 2000

Contact

Department of Biological Sciences

Physical Address:
Life Sciences South 252

Mailing Address:
875 Perimeter Drive MS 3051
Moscow, ID 83844-3051

Phone: 208-885-6280

Fax: 208-885-7905

Email: biosci@uidaho.edu

Web: Department of Biological Sciences