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Trainee Spotlight: Shawn Fahl, PhD

Shawn Fahl, PhDShawn Fahl, PhD
Postdoctoral Fellow
Dr. Dave Wiest’s Lab
Fox Chase Cancer Center
Shawn.Fahl@fccc.edu

 

 

Biography

I first became interested in a career in science during high school thanks to a very enthusiastic group of high school biology and chemistry teachers.  This led me to pursue a degree in Biotechnology from the Rochester Institute of Technology, where I was first introduced to the field of immunology.  I then attended the University of Virginia for my graduate degree, where I studied the transcriptional regulation of B cell development under the guidance of Dr. Timothy Bender.  Given my interest in studying the mechanisms that govern lymphocyte development and differentiation, I joined Dr. David Wiest’s lab at Fox Chase Cancer Center.  In addition to studying the specialized roles of ribosomal proteins in B cell development, I have also been working on the molecular mechanisms that govern the commitment of T lineage progenitors to the ∝β or γδ T cell fate.  My career goal is to continue my work into the mechanistic control of lymphocyte development, particularly at the transcriptional level, as well as how these transcriptional programs are subverted in leukemia. 

Research Overview

Ribosomal proteins are critical components required for the structure and function of the ribosome.  Recent studies, however, have suggested that ribosomal proteins have tissue-specific functions that are mediated either from within specialized ribosomes or outside of the ribosome.  In particular, we have previously demonstrated that the ribosomal protein Rpl22 is not required for global translation or life, as Rpl22-deficient mice had no defects in viability.  Loss of Rpl22, however, did result in a specific, p53-dependent block during the development of T lymphocytes.  Our current work now identifies a role for Rpl22 during B lymphocyte development.  In the absence of Rpl22, there is a significant decrease in B cell progenitors in the bone marrow and mature B cell subsets in the periphery.  This deficiency is, at least in part, due to an inability of B lineage progenitors to respond to IL-7, a key growth factor required during B cell development.  The unresponsiveness to IL-7 iss caused by enhanced expression of p53 and its downstream target genes, and loss of p53 rescues the defect in B cell development observed in Rpl22-deficient mice.  Interestingly, the control of p53 protein expression by Rpl22 is mediated post-transcriptionally, as there is no alteration in p53 mRNA expression in the absence of Rpl22.  This work provides crucial insight into the post-transcriptional mechanisms that control B lymphopoiesis and extends our knowledge of the specialized roles of ribosomal protein Rpl22 during lymphocyte development. 

Featured Publication

Shawn P. Fahl, Bryan Harris, Francis Coffey and David L. Wiest, Rpl22 Loss Impairs the Development of B Lymphocytes by Activating a p53-Dependent Checkpoint, The Journal of Immunology January 1, 2015 vol. 194 no. 1 200-209 

The Scientist Rates Fox Chase a Best Place to Work in Academia

The Scientist rates Fox Chase Cancer Center 7th on the list of Top Ten Best Places to Work Academia 2013.

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