Richard Tsika

Professor of Biomedical Sciences and Biochemistry

Email:	tsikar@missouri.edu
Phone:	(573) 884-4547
Lab:	(573) 882-4512
Fax:	(573) 884-6890
Office:	440D Bond Life Sciences Center
Mailing Address:	Biochemistry 440D Bond Life Sciences Center University of Missouri-Columbia Columbia, MO 65211
Research Areas:	Transcriptional regulation in striated muscle during development, activity, and stress; transgenic mouse models.

Educational Background

BS	Bridgewater State College	Bridgewater, Mass.	Physical Education
MS	Purdue University	West Lafayette, Ind.	Physiology of Exercise
PhD	University of California-Irvine	Irvine, Calif.	Biological Sciences

Research Description

Molecular & Cellular Biology of Muscle

My laboratory is elucidating the molecular mechanisms that control gene transcription in skeletal muscle. We are using the beta-myosin heavy chain (βMyHC) gene as our model gene since this transcribes a major contractile motor protein in striated (skeletal and cardiac) muscle, and its transcription is activated or repressed when striated muscle is subjected to altered neuromuscular activity, systemic changes in hormonal status, and as a result of certain disease states. These changes in gene expression result in profound alterations in muscle cell (fiber) phenotype as well as function.

Previously, by combining an in vivo model system (transgenic mice) and mutational analysis of the βMyHC promoter, we have identified several cis-acting elements and transcription factors that are important for basal cell-specific regulation of this gene and its response to altered neuromuscular activity.

Currently, we are: 1) using these transcription factors as bait to isolate nuclear interacting proteins, 2) analyzing how post-translational modification(s) may alter the transcriptional activity and interaction of these transcription factors with other nuclear proteins such as, chromatin remodeling enzymes, 3) utilizing mouse models ("gain" and "loss" of function) to examine the in vivo function of these transcription factors in heart and skeletal muscle during development and adult life, and 4) elucidating the intracellular signaling pathways that converge on these transcription factors.

Our studies are likely to identify novel molecular and cellular targets important for the development of new therapeutic approaches directed against muscular dysfunction associated with disease, disuse and space flight. This is important to all scientists concerned with muscle function, specialization and adaptation.

Selected Publications

R. W. Tsika, J. McCarthy, N. Karasseva, J., Y-s. Ou and G. L. Tsika. Divergence in Species and Regulatory Role of βMyosin Heavy Chain proximal promoter Muscle-CAT elements. Am. J. Physiol. Cell Physiol. 283:C1761-C1775, 2002.

N. Karasseva, G. Tsika, J. Ji, A. Zhang, X. Mao and R. W. Tsika. Transcription enhancer factor-1 binds multiple muscle MEF2 and A/T-rich elements during fast-to-slow skeletal muscle fiber type transitions. Mol.Cell Biol. 23(15):pp.5143-5164, 2003.

Parsons, S. A., D. P. Millay, B. J. Wilkins, O. F. Bueno, G. L. Tsika, J. R. Neilson, G. R. Crabtree, R. W. Tsika and J. D. Molkentin. Genetic loss of calcineurin blocks mechanical overload-induced skeletal muscle fiber-type switching but not hypertrophy. J. Biol. Chem. 279:26192-26200, 2004.

G. Tsika, J. Ji, and R. W. Tsika. Sp3 proteins negatively regulate βMyosin heavy chain gene expression during skeletal muscle inactivity. Mol. Cell Biol. 24(24):pp.10777-10791, 2004.

J. Ji, G. L. Tsika, H. Rindt, K. L.. Schreiber, J. J. McCarthy, R. J. Kelm, R. W. Tsika. Purα and Purβ collaborate with Sp3 to negatively regulate βMyHC gene expression during skeletal muscle inactivity. Mol. Cell Biol. (In Press), 2007.

Employment Opportunities

Post-Doctoral Opportunities

Electronic submission is encouraged, e-mail to biochemsearch@missouri.edu

Applicants should send CV and names of two references to:
Dr. Richard Tsika
Postdoctoral Application
Biochemistry
440D Bond Life Sciences Center
University of Missouri-Columbia
Columbia, MO 65211

Transcriptional regulation in striated muscle during development, activity, and stress; transgenic mouse models.