• Joshua Weiner, PhD

    Associate Professor, Department of Biology, The University of Iowa

    Research: “ALCAM-adhesion in development of choroid and ocular structure.”

    Brief Bio

    • B.A. with Highest Distinction in Psychology, Northwestern University, 1992
    • Ph.D. in Neuroscience, University of California, San Diego, 1999
    • Postdoctoral Fellowship with Dr. Joshua R. Sanes, Washington University School of Medicine, 1999-2004
    • Assistant Professor, Department of Biology, The University of Iowa, 2004-2011
    • Associate Professor, Department of Biology, The University of Iowa, 2011-

    My EMZ Foundation grant supported a project on the role of a cell adhesion molecule called ALCAM (Activated Leukocyte Cell Adhesion Molecule) in the retina and extra-retinal tissues. I generated the first line of mice lacking ALCAM, and found, initially, defects in both the neural retina (axon fasciculation defects) and in the pigmented, vascularized choroid, which lies behind the retinal pigment epithelium and provides blood supply to the retina. These results prompted two lines of study supported by the EMZ Foundation.

    In the first study, we tested whether ALCAM was required for correct targeting of retinal axons in their primary target in the mouse, the superior colliculus. By comparing our knockout mice with normal littermates, we showed (with collaborators from the University of North Carolina) that loss of ALCAM leads to disruptions in the mediolateral targeting of retinal axons, by disrupting a heterophilic ALCAM-L1 CAM molecular interaction. This work was published as Buhusi et al. in the Journal of Neuroscience in 2009 (reference below).

    In the second study, we examined the role of ALCAM in the motility, adhesion, and invasiveness of choroidal melanoma cell lines. ALCAM has been shown to be dysregulated in many types of cancer, including metastatic melanoma. The defects we observed in the choroid of ALCAM mutant mice led us to test ALCAM’s function in choroidal melanoma, a very severe type of cancer due to the ease with which melanoma cells can be distributed throughout the body through the richly vascularized choriocapillaris. We utilized two related lines of choroidal melanoma cells, one of which expresses ALCAM highly and is invasive and adhesive, and another with expresses low ALCAM and is not very adhesive or invasive. By using RNAi to knockdown ALCAM in the first line, and by using viral expression to misexpress ALCAM in the second line, we implicated, for the first time directly, ALCAM in the regulation of cell motility, invasiveness, and cadherin-based cell-cell adhesion. This work will be described in a paper to be submitted in Summer 2011 by Jannie, Long, and Weiner. There is no doubt in my mind that much of my early success in establishing my independent laboratory is due to the generous support of the EMZ Foundation.


    Buhusi, M., Demyanenko, G.P., Jannie, K.M., Weiner, J.A.*, Maness, P.F. * (2009). ALCAM regulates mediolateral retinotopic mapping in the superior colliculus. Journal of Neuroscience, 29:15630 –15641. (*Co-senior author) (Featured on cover).

    Jannie, K.M., Long, K., and Weiner, J.A. (2011). ALCAM regulates motility and cadherin-based adhesion in uveal melanoma cells. In Preparation.

Copyright ©2011 E. Matilda Ziegler Foundation for the Blind