Biomedical Science Department
213 Padnos Hall
Allendale, Michigan 49401
See available times here,
or by appointment
Anatomy and Physiology - BMS 202
Anatomy and Physiology Laboratory
Human Physiology - BMS 290
Human Physiology Laboratory - BMS 291
Post-doctoral fellow, University of Michigan
Ph.D. (Neuroscience) University of Michigan
B.S. (Neuroscience), B.A. (English), University of Rochester
Research in my lab centers on the transcriptional cofactor Rbpsuh which plays multiple and distinct roles in neural progenitor differentiation during different developmental stages of the nervous system. One key regulator of Rbpsuh is the Notch cell signaling pathway. However, Rbpsuh has also been shown to have Notch-independent effects as well. Previously, we’ve deleted the gene for Rbpsuh in neural stem cells of the developing mouse embryo and shown that it was Rbpsuh was necessary for the formation of astrocytes, a kind of glia, and suppressed the formation of oligodendrocytes, another kind of glia. We want to find out what acts downstream of Rbpsuh and how it exerts its effect.
An undergraduate researcher in my lab has identified novel candidate genes NfIa and Sox9, which have binding sites for Rbpsuh in their promoter regions. These genes had been shown by other labs to be necessary for stem cells to differentiate into astrocytes. Our current goal is to demonstrate that Notch or RBP-J directly binds to promoter region of these genes. The promoter binding sites on NfIa and Sox9 are unique because they have features that suggest that Rbpsuh may be able to drive gene transcription in a Notch-independent fashion.
To investigate the role of Notch, Rbpsuh and another putative co-factors that could regulate Rbpsuh on neural progenitor differentiation, another student in my lab has established an in ovo electroporation protocol and is overexpressing these genes in the developing neural tube. Now the student is asking if neural progenitors are driven to express NfIa in the presence of Notch signaling, and what role, if any, these putative co-factors have any effect on neural stem cell differentiation.
By addressing these questions, student researchers will explore multiple fields, including neuroanatomy and stem cell biology. They will be able to explore how stem cells function in vivo using many of the tools that are broadly used in developmental, cellular and gene assays, PCR, immunohistochemistry, in situ hybridization. The techniques are tractable and the answers to the questions are interesting and publishable.
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.
Page last modified September 10, 2009