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Joan Hooper, Associate Professor

Ph.D. (1983), University of California at San Francisco





Contact Info:

Molecular Biology
University of Colorado

Joan Hooper, Ph.D.  Research One South
(RC1-South), Room 12103 Phone: 303-724-3417


I am interested in the cellular and molecular mechanisms that underlie pattern formation in embryos and tissue maintenance in adults. For most of my career, I have used Drosophila as a model system to study the short range cell interactions involved in patterning, and have focused on the  Hedgehog (Hh) signaling pathway. My lab integrated genetic, molecular genetic, and biochemical approaches to ask how Hh generates dose dependent responses and how multiple signals are integrated to select different cell fates, to direct growth and morphogenesis. Most recently I have begun to apply genomics and systems biology approaches to craniofacial development.
hedgehog signaling in Drosophila
We have identified two cell surface transmembrane proteins, Patched and Smoothened, which cooperate to regulate intracellular responses to Hh (Hooper and Scott 1989, Alcedo et. al. 1996, Stone et. al . 1996). Patched transports lipids, and that activity is regulated by Hedgehog binding. The transported lipids interact with Smoothened, thereby activating downstream responses. The zinc-finger protein encoded by cubitus interruptus (ci) is the transcriptional effector of Hh signaling (Von Ohlen et. al. 1997, Von Ohlen and Hooper 1997). Ci is post-translationally regulated by Hh to become either a transcriptional repressor or a transcriptional activator. The choice is mediated by a regulatory complex which includes Costal (kinesin-like), Fused (S/T kinase) and Sufu. Smoothened controls activity of the regulatory complex via direct interaction with Costal (Ogden et al ., 2003). Moreover, two distinct activities of Smoothened control production of Ci-repressor versus Ci-activator (Hooper, 2003). More recently we identified roadkill as a gene involved in feedback inhibition of Hedgehog signaling. roadkill, a transcriptional target for Ci, encodes a protein which acts as part of an E3 ubiquitin ligase to degrade activated Ci (Kent, 2006). Most recently, we embarked on a structure-function study of the Smoothened cytoplasmic tail to delineate the phospohrylation sites and kinases responsible for the dual activities. 
ectodermal-mesenchymal interactions in mouse craniofacial development
Facial development is a complex process that involves coordinated behavior of ectoderm, endoderm and mesenchyme in three bilaterally paired facial prominences. In collaboration with Dr. Trevor Williams (UCD Craniofacial Biology) we are generating a dynamic profile of chromatin structure, transcription, post-transcriptional regulation and translation in the developing mouse face. We are applying integrated 'omics and network analyses to build a systems level description of the tissue interactions and underlying molecular mechanisms that drive facial development. Alternative splicing appears to be a key mechanism, and I am currently developing improved methods for detecting differential splicing in RNA-Seq data.


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