Merritt Taylor

Merritt Taylor
Associate Professor Biomedical Science Department 213 Padnos Hall Allendale, Michigan 49401 Phone: 616-331-8839 Fax: 616-331-2090 email: OFFICE HOURS:
See available times here,
or by appointment

BMS 202 - Anatomy and Physiology Anatomy and Physiology Laboratory BMS 290 - Human Physiology BMS 291 - Human Physiology Laboratory BMS 427 - Neuroanatomy BMS 428 - Neuroscience

Post-doctoral fellow, University of Michigan Ph.D. (Neuroscience) University of Michigan B.S. (Neuroscience), B.A. (English), University of Rochester RESEARCH INTERESTS: Neurodevelopment/Genetics/Stem Cell Biology
Our group uses the chicken and mouse embryo as model systems to determine how neural stem cell differentiation is influenced by intrinsic factors (such as gene expression) and extrinsic factors (such as factors secreted by other cells). The accessibility of the chick embryo to experimental manipulation allows us to screen for the effect of experimental manipulation on stem cell differentiation using quantitative PCR and anatomical approaches. With this approach, undergraduate and master's level students have determined that the basic helix loop helix protein Nato3 is sufficient to promote expression of markers for dopamine producing neurons. The clinical significance of this finding is that dopamine neurons are the target of degeneration in the pathophysiology of Parkinson Disease, so our current studies are focused on understanding the mechanism of this effect with the hope of informing therapeutic strategies towards this disease. Additionally, our lab is using the same model system to analyze the effect of factors outside of the neural stem cell (cell-extrinsic factors) such as polyunsaturated fatty acids. These factors have been shown to be important signaling components in development and can affect stem cell differentiation in culture, but have not been analyzed in the living embryo.

Taylor MK, Yeager K, Morrison SJ., Physiological Notch signaling promotes gliogenesis in the developing peripheral and central nervous systems. Development 2007 Jul; 134(13):2435-47 Bowen GP, Lin D, Taylor MK, Ison JR., Lesioning the auditory cortex reduces temporal acuity in the rat, and also raises noise increment thresholds. Cerebral Cortex 2003 Aug; 13(8):815-22 Taylor MK, Ahmed, R, Bagley, M, Uhler, MD., Autoinhibition and isoform-specific dominant negative inhibition of the type II cGMP dependent protein kinase. Journal of Biological Chemistry 2002 Oct; 277(40):37242-53 Stansberry J, Baude EJ, Taylor MK, Chen PJ, Jin SW, Ellis RE, Uhler MD., A cGMP-dependent protein kinase is implicated in wild-type motility in C. elegans. Journal of Neurochemistry 2001 Feb;76(4):1177-87. Taylor MK, Uhler MD., The amino-terminal cyclic nucleotide binding site of the type II cGMP-dependent protein kinase is essential for full cyclic nucleotide dependent activation. Journal of Biological Chemistry 2000 Sep 8;275(36):28053-62. Ison JR, Taylor MK, Bowen GP, Schwarzkopf SB., Facilitation and inhibition of the acoustic startle reflex in the rat after a momentary increase in background noise level. Behavioral Neuroscience 1997 Dec;111(6):1335-52. Taylor MK, Ison JR, Schwarzkopf SB., Effects of single and repeated exposure to apomorphine on the acoustic startle reflex and its inhibition by a visual prepulse. Psychopharmacology (Berl). 1995 Jul;120(2):117-27. Kellogg CK, Inglefield JR, Taylor MK, Pleger GL., Importance of hypothalamic function to stressor-induced responsiveness of the GABAA receptor in the cerebral cortex: a non-corticosterone influence. Brain Research. 1993 Apr 23;609(1-2):244-52. Kellogg CK, Taylor MK, Rodriguez-Zafra M, Pleger GL., Altered stressor-induced changes in GABAA receptor function in the cerebral cortex of adult rats exposed in utero to diazepam. Pharmacology Biochemistry and Behavior. 1993 Feb;44(2):267-73.