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Deborah Stenkamp

Deborah L. Stenkamp

Professor; Malcolm and Carol Renfrew Faculty Fellow

Office

Life Sciences South 266D

Phone

(208) 885-8963

Mailing Address

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

Research: Biomedical Science, Cellular & Molecular Biology

  • Ph.D. Neuroscience, Johns Hopkins Medical Institutions, 1993
  • B.A. Biology, Whitman College, 1987

Stenkamp’s research interests center on the examination of cellular and molecular mechanisms of vertebrate retinal development and regeneration, with a specific focus on photoreceptor differentiation, using zebrafish as the primary experimental model.

I earned my BA in Biology at Whitman College in Walla Walla, WA, then completed my PhD in Neuroscience at the Wilmer Eye Institute of Johns Hopkins Medical Institutions in Baltimore, MD. I conducted postdoctoral work at the University of Michigan in Ann Arbor, then began as Assistant Professor at the University of Idaho in 1997.

  • Stevens CB, Cameron DA, Stenkamp DL. 2011. Photoreceptor progenitors assume transient states of retinoic acid-sensitive plasticity during retinal neurogenesis. BMC Developmental Biology 11(1):51.
  • Sherpa T, Hunter SS, Frey, RA, Robison BD, Stenkamp DL. 2011. Retinal proliferation response in the buphthalmic zebrafish, bugeye. Experimental Eye Research. In press.
  • Stenkamp DL. The rod photoreceptor lineage of teleost fish. 2011. Progress in Retinal and Eye Research. In press.
  • Kashyap B, Frey RA, Stenkamp DL. 2011. Ethanol-Induced microphthalmia is not mediated by changes in retinoic acid or sonic hedgehog signaling during retinal neurogenesis. Alcoholism: Clinical and Experimental Research 35(9):1644-61.
  • Nelson SM, Mahmoud T, Beaux, M II, Shapiro P, McIlroy DN, Stenkamp DL. 2010. Toxic and teratogenic silica nanowires in developing vertebrate embryos. Nanomedicine 6(1):93-102.
  • Nelson SM, Park L, Stenkamp DL. 2009. Retinal homeobox 1 is required for retinal neurogenesis and for photoreceptor differentiation in the zebrafish. Developmental Biology 328(1):24-39.
  • Nelson SM, Frey RA, Wardwell SN, Stenkamp DL. 2008. The developmental sequence of gene expression within the rod photoreceptor lineage of the embryonic zebrafish. Developmental Dynamics 237(10):2903-17.
  • Stenkamp DL, Satterfield R, Muhunthan K, Sherpa T, Cameron DA, Vihtelic TA. 2008. Age-related cone abnormalities in zebrafish with genetic lesions in sonic hedgehog. Investigative Ophthalmology and Visual Science 49(10):4631-40.
  • Sherpa T, Fimbel SM, Mallory DE, Maaswinkel H, Spritzer SD, Sand JA, Li L, Hyde DE, Stenkamp DL. 2008. Ganglion cell regeneration following whole-retina destruction in zebrafish. Developmental Neurobiology. 68(2):166-81.

  • Photoreceptor Determination and Differentiation.
    Vertebrate vision is mediated by the function of rod and cone photoreceptors, and each species generates and maintains characteristic (adaptive) ratios of rods to cones, and of specific cone subtypes. Loss of these cells occurs in human retinal diseases that result in blindness. Zebrafish, like humans, have a duplex retina containing both rods and cones, and the cones are arranged in a regular mosaic. We use the zebrafish embryo as a model system for probing the mechanisms that regulate the determination and differentiation of the different photoreceptor types.
  • Models of Retinal Disease.
    We have identified a zebrafish genotype (syu+/-) that is associated with age-related loss of cone photoreceptors, similar to the situation in human age-related macular degeneration. Our collaborator, Dr. Brian Link (Medical College of Wisconsin) has identified another genotype (bugeye) that displays increased intraocular pressure, a characteristic of many forms of human glaucoma, and shows many retinal abnormalities. In each model, we investigate the cellular and molecular mechanisms that result in retinal pathology.
  • Retinal Regeneration.
    The mammalian retina responds to damage by launching a gliotic response, while the zebrafish retina launches a regenerative response. Interestingly, the major glial cell type of the retina (Müller glia) is involved in mediating both responses. We evaluate the role of different damage modes in influencing the ultimate ‘success’ of the regenerative response, and we are probing the extent to which retinas experiencing pathology of a genetic basis can also regenerate.

  • 2011 fall: Visual System guest lecturer, Accelerated Biology course at Moscow High School.
  • 2011 summer: Beyond Baccalaureate Panel, Annual INBRE conference.
  • 2010 fall: “A Bird’s Eye View: Adaptations of the Avian Visual System” Presentation for Semester at Sea (University of Virginia).
  • 2009 summer: “Neurogenesis” Interview for GoCognitive! Web instructional tool.
  • 2008 spring: “What do Animals See?” Presentation for Palouse Discovery Science Center.

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