Dr. Reecy s areas of research include gene function, mechanisms of gene expression during vertebrate development, and beef cattle molecular genetics.

The stretching of skeletal muscle induces hypertrophy of myofibers and myotubes in vitro and in vivo. Myofiber hypertrophy is a result of increase in cell size due to increased muscle protein accretion and recruitment of satellite cells. The hypertrophic signal is intrinsic, as it is mainly, the exercised muscle that under goes hypertrophy and not all the muscles of the limb or the whole body. It is important to discover the intra-cellular pathways involved in mechanotransduction. Knowledge of the intracellular signaling pathways will help develop new therapeutic strategies to produce muscle hypertrophy to enhance lean deposition in livestock or to prevent muscle atrophy from AIDS, sarcopenia, spinal cord injury, limb immobilization, chemotherapy, cachexia, malnutrition, and frailty. Toward this goal, we were the first to report on global changes in gene expression that accompany work overload hypertrophy. We have gone on to demonstrate functional roles for genes that are differentially expressed.

Double-muscling in cattle is the result of inactivation of myostatin. Recently, myostatin was knocked out in mice, which results in a 200% increase in muscle mass. Recently, progress has been made into the elucidation of intracellular signaling mechanisms controlled by myostatin. Recently, we reported that Wnt4 and sFRPs lie downstream of myostatin and are most likely involved in regulation of satellite cell proliferation. Furthermore, we quantitated gene expression levels in wild-type and myostatin-null mice during primary myotube formation, secondary myotube formation, as five weeks postnatal. Interestingly, gene expression changes could be binned into any phenotype one was interested with respect to muscle growth. We have gone onto evaluate the role that myostatin plays in work overload hypertrophy, skeletal muscle atrophy, and recovery from skeletal muscle atrophy. Recently, we initiated an experiment with myostatin-null mice and M16i obese mice to identify epistatic alleles that control skeletal, skeletal muscle, and adipose growth. Considerable resources have been devoted to identifying genes in important agricultural species by expressed sequence tag (EST) sequencing. A major aim in genomics is to understand biological function and diversity by identifying similarities and differences between species. As part of a consortium, we are working with researchers at University of Missouri, University of Minnesota, and Texas A&M University to develop and characterize a 24,000 long-oligo array. Another objective of the lab is to identify and analyze genes that play a major role in the genetic variation in quantitative traits in livestock. A major thrust of worldwide research currently is the development of well-ordered informative maps for domestic species. Comparative information from other species at the molecular and genomic level is used to clone and study genes believed to play a role in growth, development, and meat quality in beef cattle. We are focusing on the identification of molecular markers associated with animal health (pinkeye and respiratory disease), carcass traits, and the healthfulness of meat. We have determined the extent to which genetics controls variation gene resistance to pinkeye and fatty acid compositions of meat. We are currently expanding this research to evaluate resistance to respiratory disease and other nutrients in meat.

Livestock geneticists have done a wonderful job of identifying regions of the genome that are associated with traits of economic importance. However, they have identified to many QTLs that it is no longer feasible for researchers to stay abreast of all publications. To alleviate this problem, we have developed a livestock QTL database where we have curated cattle, chicken and pig QTL. We are working to expand this resource to allow researchers to seamlessly move from QTL information to genomic information to assist them in the identification of causative alleles underlying QTL. As a result of this work, we realized there is a large need to develop a standardized nomenclature for phenotypes. Toward this end, we have developed resources to allow for the collaborative development of a phenotype ontology. We are currently working with the rat and mouse communities to expand this resource to allow for the exchange of genomic and phenotypic information across species.

Zhi-Liang, H., E.R. Fritz, and J.M. Reecy. 2006. AnimalQTLdb: A Livestock QTL Database Tool Set for Positional QTL Information Mining and Beyond. Nucleic Acid Research Database issue doi:10.1093/nar/gkl946.

Tuggle, C.K., J.C.M. Dekkers, and J.M. Reecy. 2006. Integration of structural and functional Genomics. Animal Genetics 37:(Supplement 1):1-6.

Tantia, M.S., R.K. Vijh, S.T. Bharani Kumar, B. Mishra, and J.M. Reecy. 2006. Comparative analysis of GDF 8 (myostatin) in Bos indicus and Bos Taurus. DNA Sequence (In Press).

Bao, J., Z. Hu, D. Caragea, J.M. Reecy, and V. Honavar. A Tool for Collaborative Construction of Large Biological Ontologies. Fourth International Workshop on Biological Data Management (BIDM 2006), Krakov, Poland, IEEE Press. pp. 191-195

Steelman, C. A., J.C. Recknor, D. Nettleton, and J.M. Reecy. 2006. Transcriptional profiling of myostatin-knockout mice implicates Wnt signaling in postnatal skeletal muscle growth and hypertrophy. FASEB Journal 20(3):580-582. Epub 2006 Jan 19.

Hu, Z.-L., S. Dracheva , W. Jang, D. Maglott, J. Bastiaansen, M.F. Rothschild, and J.M. Reecy. 2005. A QTL Resource and Comparison Tool for Pigs: PigQTLDB. Mammalian Genome 15: 792-800.

J.M. Reecy, D. Moody-Spurlock, and C. H. Stahl. 2005. Gene expression profiling: Insights into skeletal muscle growth and development. Journal of Animal Science 84(E. Suppl.):E150–E154.

Hu, Z.-L., K. Glenn, A.M. Ramos, C.J. Otieno, J.M. Reecy, and M.F. Rothschild. 2005. Expeditor: A pipeline for designing primers Using Human Gene Structure and Livestock Animal EST Information. Journal of Heredity 96:1-3.

Kim, K.-S., J.M. Reecy, W.H. Hsu, L.L. Anderson, and M.F. Rothschild. 2004. Functional and phylogenetic analyses of a melanocortin-4 receptor mutation in domestic pigs. Domestic Animal Endocrinology 26:75–86.

Washington, T.A., J.M. Reecy, R.W. Thompson, L.L. Lowe, J.M. McClung, and J.A. Carson. 2004. Lactate dehydrogenase expression at the onset of altered loading in rat soleus muscle. Journal of Applied Physiology 97:1424-1430.