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UW-Madison School of Medicine and Public Health
Medical Microbiology and Immunology

The Huttenlocher Lab

The Huttenlocher lab studies the basic molecular mechanisms that regulate cell migration and is interested in how defects in cell migration contribute to human disease. To migrate cells extend leading edge protrusions, stabilize adhesions and subsequently detach from the cell's rear. We are interested in how adhesions are regulated at both the leading and trailing edge of migrating mesenchymal and amoeboid cells.

The picture shows vinculin (green) containing focal adhesions and actin stress fibers (red) in a fibroblast like cell. The Huttenlocher laboratory studies how adhesion dynamics are regulated. We are interested in the dynamics of both focal adhesions and degradative structures including podosomes and invadopodia.

The Huttenlocher laboratory uses zebrafish to study cell migration and inflammation in vivo.

Tissue wounding induces the recruitment of neutrophils to the wound and subsequent reverse migration back toward the vasculature. Cell tracks show live imaging of GFP positive neutrophils from the vasculture to the wound and back toward the vasculature.

We have performed genetic screens for zebrafish mutants that exhibit chronic inflammation and infiltration of immune cells into the epidermis. Shown here in situ for zebrafish neutrophil myeloperoxidase. The bottom panel shows a zebrafish line identified in a screen for chronic inflammation mutants.

A major focus for the laboratory is to understand how cell signaling is regulated during chemotaxis of leukocytes in vivo. The image shows an overlay of sequential ratiometric images to show the polarization of PI3K signaling as neutrophils are migrating in vivo.

A major challenge for our research group is to understand the mechanisms that regulate bidirectional trafficking of leukocytes to and from inflamed tissue in vivo. We observed reverse migration of neutrophils from tissues back toward to vasculature to resolve inflammatory responses. We are now studying the mechanisms that regulate this reverse migration.

The schematic shows cell signaling neutrophil neutrophil chemotaxis in vivo. We have observed dynamic F-actin at the leading edge and more stabilized F-actin at the uropod (Yoo, Developmental Cell, 2010).

             To contact us:

Huttenlocher Lab, Department of Medical Microbiology
University of Wisconsin-Madison
1550 Linden Drive, Room 4225
Madison, WI 53706-1532

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