Office: (217) 244-4183
Lab: (217) 244-4512
Mail to: University of Illinois
Chemical and Life Sciences Laboratory
601 S. Goodwin Ave. Room B107
Urbana IL 61801-3761
Assistant Professor of Cell and Developmental Biology
Development, Pattern Formation, Regulation of Gene Expression, Signal Transduction
B.A., Harvard University
Ph.D., Stanford University
Postdoctoral fellow, University of California Berkeley
Wound repair and tissue regeneration; Drosophila genetics; Development and patterning
After wounding or injury some organisms, tissues and organs carry out an elegant process of regeneration to repair and replace the lost tissue. By studying model systems that regenerate well we can understand the mechanisms that promote regeneration and use them to manipulate healing and re-growth in critical human organs.
The process of regeneration involves a series of steps, each of which is poorly understood. Some outstanding questions are: How does a tissue sense damage? How does a damaged tissue initiate new growth? How is regenerative growth constrained so that it replaces only what was lost? How are cell fates properly specified within the new tissue? My lab aims to answer these questions using the regeneration of a simple epithelial tissue in the model organism Drosophila melanogaster.
We are using a novel method to induce tissue damage and regeneration in the developing Drosophila wing using genetic tools. Using this method I showed that damaged tissue dramatically alters its expression of signaling molecules such as Wingless (Wnt) and Dpp (BMP) as well as transcriptional regulators such as Vestigial and Myc. Furthermore, Wg and Myc play a crucial role in coordinating regenerative growth.
My lab is now conducting a forward genetic screen for mutations that impair tissue regeneration, and are identifying genes required for each step of the regeneration process. Current work involves the characterization of several genetic loci required for regenerative growth after damage - mutants have small and poorly-regenerated wings, as well as several loci that fail to re-pattern appropriately and correctly specify cell fates within the regenerated tissue - mutants have fully regenerated wings that are improperly shaped and patterned.
In addition to the genetic screen, we are developing the ability to conduct live imaging of regenerating tissue and to carry out systems-level analyses of the cellular and transcriptional changes that occur after tissue damage. Our goal is to uncover the mechanisms that regulate regenerative tissue repair, enabling us to induce, manipulate or enhance regeneration after injury.
Roy J. Carver Charitable Trust Young Investigator Award
Rachel K. Smith-Bolton. (2014). Drosophila imaginal discs as a model of epithelial wound repair and regeneration. Advances in Wound Care. doi:10.1089/wound.2014.0547.
Rachel K. Smith-Bolton, Melanie Worley, Hiroshi Kanda, and Iswar K. Hariharan. (2009). Regenerative growth in Drosophila imaginal discs is regulated by Wingless and Myc. Developmental Cell. 16(6): 797-809.
Leslie A. Jarvis*, Stephanie J. Toering*, Michael A. Simon, Mark A. Krasnow, and Rachel K. Smith-Bolton*. (2006). Sprouty proteins are in vivo targets of Corkscrew/SHP-2 tyrosine phosphatases. Development. 133(6): 1133-42. *These authors contributed equally to this work.
Rachel K. Smith, Pamela M. Carroll, John D. Allard, and Michael A. Simon. (2002). MASK, a large ankyrin repeat and KH domain-containing protein involved in Drosophila receptor tyrosine kinase signaling. Development. 129(1): 71-82.