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Linda Barlow, Ph.D.

Professor

Linda Barlow Anschutz Cell Developmental Biology
 linda.barlow@cuanschutz.edu
 303-724-3438
 Ph.D., University of Washington - Seattle, 1991
 Rocky Mountain Taste and Smell Center

Graduate Program Affiliations:

Biomedical Sciences Program

Cell Biology, Stem Cells, and Development

Medical Scientist Training Program (MSTP)

Neuroscience Graduate Program

We rely upon our sense of taste to discern nutritious and delicious from spoiled food or even potentially toxic items. Taste buds are composed of a heterogeneous collection of sensory receptor cells, which transduce sweet, bitter, umami (savory), salt and sour into electrochemical signals that are transmitted by nerve fibers to the brain.

Barlow Lab -- Figure 2 (300 x 492)

One particularly intriguing aspect of the taste system is that taste bud cells are continually renewed throughout life, in contrast to most of our peripheral sensory receptor cells such as rods and cones or hair cells of the inner ear, which lack this capability. Yet despite this regular turnover, our sense of taste is remarkably constant – sweet or salty foods eaten last year, when eaten today still taste sweet or salty. Intriguingly, taste function is often distorted in patients receiving targeted irradiation for head and neck tumors, as well as in cancer patients treated with a variety of specific chemotherapeutics, suggesting that taste cell turnover may be perturbed.

Finally, different people have different taste preferences, and this variability, in part, may reflect the number of taste buds found on the tongue. For example, “super tasters” appear to have an overabundance of taste buds, which occupy a large portion of the tongue surface, while most of us have taste buds distributed much less densely. 

Thus, work in the lab focuses on 3 large questions, each of which is supported by a current NIH grant:

  1. How is the pattern, and therefore number, of taste buds established during embryonic development?
  2. Once established, how are taste bud cells continually renewed in adults?
  3. How do cancer therapies cause taste dysfunction?

We use both embryonic and adult mice to test hypotheses related to these main questions. Specifically, we employ drug-inducible, tissue-specific molecular genetics in mice to map the fate of subsets of cells in embryos and adults, as well as to delete or augment gene function in targeted cell populations. We evaluate the outcomes of these molecular genetic manipulations using a combination of immunofluorescence and in situ hybridization with antisense RNA probes assessed via conventional fluorescence microscopy, or spinning disc and laser scanning confocal microscopy.

We also employ quantitative PCR to determine how gene expression levels are altered in induced mutants compared with genetic controls. Additionally, we are gaining expertise in the powerful MATLAB platform to pursue more rigorous and automated quantitative analyses. Most recently, we have developed protocols for FACS to separate taste bud generating epithelial cells from non-sensory tongue epithelium, with the short term goal to use RNAseq to define and compare the transcriptomes of these two populations.

We also employ injury models to understand how the adult taste receptor cells regenerate, and gain insight into how taste function is perturbed in cancer patients. Toward this end, we have developed a mouse model of head and neck irradiation (Nguyen, Reyland and Barlow, 2012. J Neurosci), and are piloting similar studies using chemotherapeutics.

Barlow Lab -- Figure 1