Education

• Post-doctoral fellowship (2000) University of Chicago, Developmental Biology
• Cold Spring Harbor Summer Course Molecular Biology (1995)
• PhD (1994) Arizona State University, Developmental Biology
• MS (1991) Arizona State University, Developmental Biology
• BS (1989) Arizona State University, Biology

Research Interest

Stem cells, stem cells, stem cells!! They’re the main focus of the Gallicano laboratory. We use a number of methods and approaches including molecular (such as analyzing microRNAs and their role in development), ultrastructural, and biochemical tools to determine how pleuripotent embryonic stem (ES) cells, multi-potent adult stem cells, and totipotent single cell mammalian embryos differentiate into all the cells of the body. The idea of stem cell based therapies is particularly prevalent in the fields of diabetes, cardiac and neurological disorders. These diseases are particularly good targets for stem cell therapies because the majority of the symptoms are associated with the loss of one specific cell type, e.g., the dopamine (DA) neuron for Parkinson’s disease (PD), or ?-islet cells for diabetes. While the potential use of ES cell derived terminally differentiated cells types as therapies is promising, there are several problems that must be addressed. These problems include formation of teratomas, grafting efficiency, differentiation capacity, incorporation into existing tissue (i.e., synapse formation for neurons or grafting potential of cardiomyocytes), and immunological response. However, substantial research and promise is growing using human adult stem cells derived from cord blood, bone marrow or the new induced pleuripotent stem cells (iPS). Though it is currently believed that adult stem cells are not as flexible as ES cells, it might be possible to apply the knowledge gained from research on ES cells to trans-differentiate significantly more adult stem cells into embryonic-like cardiomyocytes for therapeutic use.

A secondary focus of my lab is cellular adhesion during early embryogenesis in mammals. We use three distinct biological disciplines, Confocal and Electron Microscopy, Molecular, and Biochemical analyses, all of which have begun to shed light on the importance of certain components involved with cellular adhesion in the embryo. One specific cell adhesion component we work on is desmoplakin, a major building block of junctions known as desmosomes. These junctions act like spot welds between cells, providing areas of tight and rigid adhesion between cells in tissues and organs that undergo a great deal of mechanical stress (e.g., heart, skin, early embryonic tissue, others). To study desmoplakin in detail we have used embryonic stem cell technology to "knock out" the desmoplakin gene in mice. Embryos that lack desmoplakin die about 6 days after fertilization because they fail to expand their egg cylinders (the main structure that houses the embryo in the uterus). The cells of the egg cylinder in desmoplakin null mice basically fall apart. Numerous other problems (e.g., decreased cellular proliferation) also are found in these early stage embryos lacking desmoplakin and we are currently trying to determine how the loss of desmoplakin causes these problems during development.

Selected Publications

Gallicano, G.I., P. Kouklis, C. Bauer, M. Yin, V. Vasioukin, L. Degenstein, and E. Fuchs. (1998). Desmoplakin is required early in development for assembly of desmosomes and cytoskeletal linkage. Journal of Cell Biology 143:2009-2022. COVER PHOTOGRAPH

Gallicano, G.I., Bauer, C., and Fuchs E. (2001) Rescuing Desmoplakin Function in extraembryonic ectoderm reveals an importance for desmoplakin in embryonic heart, neurepithelium, skin, and vasculature. Development, 128(6) 929-941.

Gallicano, G.I., (2001). Composition, regulation, and function of the cytoskeleton in mammalian eggs and embryos. Frontiers in Bioscience (6:d1089-1108).

Zhou, X., Quann, E., Gallicano, G.I., (2003) Differentiation of non-beating embryonic stem cells into beating cardiomyocytes is dependent upon down regulation of PKC? and ? in concert with up regulation of PKC? Developmental Biology 255:407-422.

Zhou , X., Stuart, A., Dettin, L., Rodriguez, G., and Gallicano, G.I. (2004). Desmoplakin is required for microvascular tube formation in culture. Journal of Cell Science 117:3129-3140 (An Evaluated and Recommended Article by the Faculty of 1000 http://www.facultyof1000.com).

Foshay, K., Rodriguez, G., Hoel, B., Narayan, J., Gallicano, G.I. (2005) JAK2/STAT3 controls cardiomyocyte differentiation in vitro (Stem Cells. 23:530-543).

G. Ian Gallicano, Kara Foshay, Yolande Pengetnze, and Xuan Zhou. (2005) Dynamics and unexpected localization of the plakin binding protein, kazrin, in mouse eggs and early embryos. (Developmental Dynamics. 234(1):201-14).

Zhou X., and Gallicano, G.I. (2006) Microvascular Tubes Derived from Embryonic Stem Cells Sustain Blood Flow (Stem Cells and Development, 15:335-347 (Cover Photograph).

Jonathan R. Slotkin, Lina Chakrabarti, Hai Ning Dai, Rosalind S.E. Carney, Barbara S. Bregman, G. Ian Gallicano, Joshua G. Corbin, Tarik F. Haydar. (2007) In vivo quantum dot labeling of mammalian stem and progenitor cells. (Developmental. Dynamics. 2007; 236(12):3393-401)

Foshay, K., and Gallicano, G. I. STAT3 Regulates Sox2 During Neural Precursor Cell Differentiation. (In Press April 2008 Stem Cells and Development).

Foshay, K., Miera, A., Stuart, A., Fingland, N., Mobley, S., Gallicano, G.I. (2007) Unraveling the complex nature of prostate cancer stem cells. Cancer Biomarkers. 3(4-5):233-44.

Foshay, K., and Gallicano, G.I. Regulation of Sox2 by STAT3 Initiates Commitment to the Neural Precursor Cell Fate. (2007) Current Stem Cell Research and Therapy. 2(4):264-71).

Foshay, K., and Gallicano, G. I.* MicroRNAs Regulate the Onset of ES Cell Differentiation via Inhibition of STAT3 (In Press April 2008 Stem Cells and Development).

Cashman, Kathleen A., Muralidhar, Sumitra, Gallicano, G. Ian., Rosenthal, Leonard J*. HHV8 ORF K12 oncogene is embryonic lethal, and induces vascular pathology through upregulation of both VEGF ligand and its receptor, Flk-1 (submitted to Oncogene).

Mobley, S., Foshay, K., Michelle Park, and Gallicano, G.I.* Downregulation of PKG and PKC enhances differentiation of non-beating embryonic stem cells into beating cardiomyocytes (submitted to Stem Cells)