Education
Columbia University, Ph.D. 1998

Biography
Dr. Berrier received her Bachelor of Science Degree in Chemistry from Lafayette College in 1990. She earned her doctorate in microbiology from Columbia University in 1998, studying mechanisms of regulating leukocyte gene expression during both cellular and humoral immune responses. During her postdoctoral fellowship at Albany Medical College in the laboratory of Dr. LaFlamme, she studied the role of the integrin b-tail in regulating both forskin fibroblast and epithelial cell adhesive function and signaling. In 2004, she joined the LSU Health Sciences Center School of Medicine as an assistant professor in the Department of Cell Biology and Anatomy. Shortly thereafter, she joined the Louisiana Cancer Research Consortium and was named a Distinguished Faculty Member of the LSUHSC-NO School of Dentistry, Center of Excellence in Oral and Craniofacial Biology. After Hurricane Katrina, she worked on cell-matrix biology in the laboratory of Dr. Yamada at NIDCR/NIH as a Katrina Visiting Faculty Scholar sponsored by NCMHD/NIH. Dr. Berrier joined the School of Dentistry as an assistant professor in the Department of Oral and Craniofacial Biology with a secondary appointment in the Department of Pharmacology and Experimental Therapeutics in 2008.

Research Interests
The molecular and cellular events that induce conversion from normal oral epithelial to invasive oral squamous carcinoma are not completely understood. The aim of research in the Berrier lab is to further understand the cellular machinery that promotes oral tumor metastasis. The role of cell-matrix interactions in oral cancer is an area of particular interest because proteins in matrix adhesions are known to perform important functions in tumor progression, proliferation and invasion. Integrins are the principle cell surface receptors that mediate cell-matrix adhesion and if the function of these integrin receptors is disrupted, then reductions in oral cancer tumor metastasis are observed. Based upon the important role of integrins in oral cancer tumorigenesis, one project area in the lab focuses on determining whether integrin receptors on the cell surface selectively recruit particular cytoplasmic effector proteins during oral cancer tumor invasion. A second project area involves determining whether the tumor matrix can be bio-engineered to reduce the invasive potential of oral tumor cells that reside within a tumor microenvironment. Both projects will potentially provide future alternative approaches to reduce the invasive nature of oral tumors.

Research Interests--Keywords
Oral cancer, cell-matrix biology, cell adhesion, cell migration, cell signaling, tumor cell invasion, tumor cell proliferation and metastasis, bio-engineering the extracellular matrix

Teaching Activities
Dental Hygiene Pharmacology DHY4101, Co-Director
Dental School Residents-Research Methods Oral Biology 202
School of Medicine Graduate School-Cell Signaling and Cell Cycle control- CMB-D

Selected Publications
A.L. Berrier, A.M. Mastrangelo, J. Downward, A. Toker, M. Ginsberg and S.E. LaFlamme. Activated R-Ras, Rac1, PI 3-kinase, and PKCe can each restore cell spreading inhibited by isolated integrin b1 cytoplasmic domains. J. Cell Biol. 151: 1549-1560, 2000.

A.L. Bodeau, A.L. Berrier, A.M. Mastrangelo, R. Martinez and S.E. LaFlamme. A Functional comparison of mutations in integrin b1,3 cytoplasmic domains: Effects on the regulation of tyrosine phosphorylation, cell spreading, cell attachment and b1 integrin conformation. J. Cell Sci. 114: 2795-2807, 2001.

A.L. Berrier, R. Martinez, G.M. Bokoch, and S.E. LaFlamme. The integrinb tail is required and sufficient to regulate adhesion signaling to Rac1. J. Cell. Sci. 115:4285-4291, 2002.

A.L. Berrier, K.M. Yamada. Mini-Review. Cell-Matrix Adhesion. J Cell. Physiol. 213:565-573, 2007.

A.L. Berrier, C.W. Jones, S.E. LaFlamme. Tac-b1 inhibits FAK activation and Src signaling. Biochem Biophys Res Comm, 368:62-67, 2008.

J.A. Green, A.L. Berrier, R. Pankov, K.M. Yamada. b1 integrin cytoplasmic domain residues selectively modulate fibronectin matrix assembly and cell spreading by differentially regulating Talin and AKT. J. Biol. Chem. 284(12):8148-59, 2009.