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A discovery of potential importance to cystic fibrosis therapy

Hidden signals in a well-studied gene

November 9, 2009 — For the past 20 years, regulatory mechanisms controlling a large gene that is mutated in cystic fibrosis (CF) patients have eluded scientists. CF is a severe genetic disease that results in lung damage and nutritional deficiencies. Mutations in the cystic fibrosis transmembrane conductance regulator (CFTR) cause changes in the airway surface liquid that produce a thick mucus layer. This results in colonization by bacteria, which acquire antibiotic resistance and become increasingly difficult to eradicate. Although treatments for CF patients have improved, therapeutics that target the underlying CFTR defect could make a major difference to the health and longevity of these individuals.

In a study published online on November 6, 2009, in the Proceedings of the National Academy of Sciences of the United States ofAmerica (PNAS), the laboratory of Ann Harris has found that the CFTR gene adopts a very specific three-dimensional conformation in cells that express the gene and thus are affected by the disease. In cell types where the gene is silent this conformation does not exist. The genetic elements that coordinate this conformation lie at large distances from each other, and thus the discovery and characterization of these elements and the proteins that interact with them will likely have important implications for CF therapeutics that aim to boost expression of the gene in specific cell types, either by gene therapy or by pharmacological methods. Moreover, this study offers a framework for the discovery of distal genetic elements that regulate the expression of other disease-causing genes.

The first author is Christopher Ott, a graduate student in the Harris laboratory and a member of the Integrated Graduate Program in the Life Sciences (IGP) at Northwestern University. The other authors in the Harris laboratory are Neil Blackledge, a former graduate student and postdoctoral fellow; Jenny Kerschner, IGP graduate student; and Shih Hsing Leir, postdoctoral fellow. Collaborators are Dr. Greg Crawford of Duke University and Dr. Calvin Cotton of Case Western University. Ann Harris, PhD, is Professor of Pediatrics and the Valerie and George D. Kennedy Endowed Chair in Human Molecular Genetics, Northwestern University’s Feinberg School of Medicine; and the director of the Human Molecular Genetics Program of Children’s Memorial Research Center.

Children’s Memorial Research Center is the research arm of Children's Memorial Hospital, the pediatric teaching hospital for Northwestern University's Feinberg School of Medicine.  The research center is also one of 29 interdisciplinary research centers and institutes of the Feinberg School, where principal investigators who are part of the research center are full-time faculty members. Built upon a team approach, the research center generates knowledge that will lead to cures for the diseases of children with additional focus on the pediatric precursors of adult diseases. The research center actively encourages a synergy of ideas among physician scientists, basic scientists, technicians, nurses and trainees in various disciplines. Its thematic research programs bridge gaps between the biomedical, clinical and social sciences and provide an environment to accomplish common goals.

For more information contact Peggy Jones, Children’s Memorial Research Center at 773.755.6341 or pmjones@childrensmemorial.org. 



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