Michele A. Battle, PhD

Michele A. Battle, PhDAssociate Professor

Medical College of Wisconsin
Department of Cell Biology, Neurobiology & Anatomy
8701 Watertown Plank Road
Milwaukee, WI 53226-3548

(414) 955-8089
(414) 955-6517 (fax)

PhD, Michigan State University, East Lansing, Michigan, 2002
BS, University of Scranton, Pennsylvania, 1996

Research Area

Transcriptional control of gut development and function

It has long been known that the small intestinal epithelium carries out different functions along its anterior to posterior axis. For example, the jejunum is a major site for nutrient uptake, whereas the ileum primarily absorbs bile salts. The mechanism by which these specific regions of the small intestine gain their characteristic functions, however, is unknown. Elucidating this process is critical to our ability to restore function to intestinal tissue damaged by disease or injury. We propose that the repertoire of transcription factors expressed in any given intestinal region drives the establishment and maintenance of that region’s characteristic function through the activation and repression of downstream targets. Although many important transcription factors have been identified in the small intestinal epithelium including the zinc finger transcription factors GATA4 and GATA6 and the homeobox transcription factors PDX1, CDX1, CDX2, and HNF1α, the in vivo contribution these factors make to intestinal regionalization remains largely uncharacterized. The long-term goal of the Battle laboratory is to elucidate the transcriptional regulators and the signal transduction pathways required to generate and sustain the functional specificity of discrete regions of the small intestine. Our current work seeks to define the mechanisms through which GATA4 and GATA6 work independently and in concert to establish and maintain intestinal function. Six GATA family proteins have been described in vertebrates, and GATA4, GATA5, and GATA6 are the members of this family expressed in the gastrointestinal tract. Both Gata4 and Gata6 knockout mice die during embryonic development before the intestine forms because of defects in the extraembryonic endoderm. This tissue shares similar function with the GI tract in that it expresses a similar set of genes and is responsible for maintaining the optimal nutrient balance for the developing embryo. Mice lacking Gata5, however, displayed abnormalities only in the female genitourinary tract. Because Gata5 knockout mice manifested such a limited phenotype and no disruption to the gut, we have focused on uncovering the roles that GATA4 and GATA6 play in intestinal development and function. Our recent work demonstrated that GATA4 is essential for jejunal function and confirmed that GATA4 plays a pivotal role in determining jejunal verus ileal identity (Battle et al., 2008 Gastroenterology).


Battle Lab
Michele A. Battle, PhD, Laboratory

Emily Walker, Cayla Thompson, Michele Battle & Bridget Kohlnhofer

Recent Publications

Medical College of Wisconsin
8701 Watertown Plank Road
Milwaukee, WI 53226
(414) 955-8296
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