Assistant Medical Professor
Dr. Juarez is Assistant Professor in the Department of Microbiology and Immunology at the Sophie Davis School of Biomedical Education. Previously, she was Assistant Project Scientist at the University of California, San Diego, and NIH-NIGMS IRACDA fellow. Dr. Juarez is a member of the American Society for Cell Biology, Genetics Society of America, and the Society for Developmental Biology.
Ph.D., 2004, State University of New York, Stony Brook
B.S., 1998, University of California, Berkeley
Epidermal wound response and Drosophila Genetics
Dr. Juarez studies how an epidermal wound provides signals that initiate a variety of localized responses. The wound response signals promote regeneration and repair the breach in the epidermal barrier. The Drosophila melanogaster embryonic epidermis provides an excellent system to discover new genes that regulate wound-healing processes.
Using fluorescent epidermal "wound" reporters that are locally activated around wound sites, we utilize the powerful genetic tools of Drosophila to identify mutants required to activate or delimit wound-induced transcriptional responses to a local zone of epidermal cells. Recent studies reveal a new role for the genes Dual oxidase, Flotillin-2 and Src42A to regulate the spread of wound-response reporters.
Combining puncture wound technique with microinjection, we efficiently test the wound response triggered by chemical compounds. We found that four biochemical treatments (a serine protease, a Src kinase inhibitor, methyl-ß-cyclodextrin, and hydrogen peroxide) are sufficient to globally activate epidermal wound response genes in Drosophila embryos. These results define new functions of well-conserved genes, and the interactions among them, which regulate the local transcriptional response to puncture wounds.
Current projects focus on the mechanism of endocytosis to promote wound signal turnover during the epidermal wound response and investigating the role of novel wound response regulators during other stages of wound healing.
Pongsawakul PY, Juarez MT, Zhang EE, Hirota T, Kay SA. The role of cytoplasmic CRYPTOCHROME in repressiong cAMP signaling. (In Prep)
Juarez MT, Patterson RA, Li W, McGinnis W. Microinjection wound assay and in vivo localization of epidermal wound response reporters in Drosophila embryos. (In Revision)
Patterson RA, Juarez MT, Hermann A, Sasik R, Hardiman G, McGinnis W. Serine Proteolytic Pathway Activation Reveals an Expanded Ensemble of Wound Response Genes in Drosophila (In Revision)
Paré A, Kim M, Juarez MT, Brody S, McGinnis W (2012). The functions of Grainy head family proteins in animals and fungi and the evolution of apical extracellular barriers. PLoS ONE 7(5): e36254.
Juarez, MT, Patterson RA, Sandoval-Guillen E McGinnis W (2011). Duox, Flotillin-2, and Src42A are required to activate or delimit the spread of the transcriptional response to epidermal wounds in Drosophila. PLoS Genetics 7(12):e1002424.
Pearson JC, Juarez MT, Kim M, Drivenes Ø, McGinnis W (2009). Multiple transcription factor codes activate epidermal wound-response genes in Drosophila. PNAS 106(7), 2224-2229.
Nogueira FT, Madi S, Chitwood DH, Juarez MT, Timmermans MCP (2007). Two small regulatory RNAs establish opposing fates of a developmental axis. Genes and Development 21(7), 750-755.
Juarez MT, Kui JS, Thomas J, Heller BA, Timmermans MCP. (2004) microRNA mediated repression of rolled leaf1 specifies maize leaf polarity. Nature 428(6978), 84-88.
Juarez MT, Twigg RW, Timmermans MCP (2004). Specification of adaxial fate in the maize leaf. Development 131(18) 4533-4544.
Timmermans MCP, Juarez MT, Phelps-Durr TL (2004). A Conserved microRNA signal specifies leaf polarity. Cold Spring Harbor Symposia on Quantitative Biology, 69, 409-417.
Ori N, Juarez MT, Jackson D, Yamaguchi J, Banowetz GM, Hake S. (1999) Leaf senescence is delayed in tobacco plants expressing the maize homeobox gene knotted1 under the control of a senescence-activated promoter. Plant Cell 11, 1073-1080.