Prior to 1989, very little was known about the specific defect causing CF. It did not appear to be caused by a pathogen, like the diseases you are working on in this week’s Discussion For
Prior to 1989, very little was known about the specific defect causing CF. It did not appear to be caused by a pathogen, like the diseases you are working on in this week’s Discussion Forum. Instead, CF is caused by defects called mutations in a gene inherited from the parents of the affected individual. We will study the genetic aspects of CF in a later chapter.
The discovery of the gene associated with the CF disorder in 1989 was a tremendous triumph at the time, as medical researchers did not have a clear understanding of the function of the gene before this discovery. It was quite an exciting story! The gene was found to direct the synthesis of a membrane transport channel protein, similar to the potassium ion channel which is shown in your textbook and displayed at the top of this page. This protein is now referred to as the Cystic Fibrosis Transmembrane Conductance Regulator, abbreviated CFTR. To learn more about this protein, its structure, how it normally works, and how it is defective in CF patients, review the following webpages and try to relate this information to Chapter 3 content. The first webpage from the Cystic Fibrosis Foundation reviews the Basics of the CFTR Protein, and the second webpage from the Johns Hopkins Cystic Fibrosis Center covers the Structure and Function of the CFTR Protein.
3. Regarding the CFTR protein found in a normal individual, where would you find this protein located in a lung cell, what solute does this protein transport, and in what direction does the transport normally occur relative to the cell?
4. Regarding the CFTR protein found in a normal individual, this protein channel is involved in passive transport. Relate what this means in terms of what you’ve learned in Chapter 3. Specifically, does it require ATP for energy to function, and does the solute move from low to high concentration or from high to low concentration across the membrane?
5. Regarding the CFTR protein found in individuals with CF, relate how the defective CFTR in the lung cells can actually lead to the symptoms in the lungs that you described in question 2 above?
6. Several classes of mutations to the CFTR protein were mentioned in the Johns Hopkins webpage. Choose one, for example the Class 2 Mutations, and discuss how that class of mutation impacts the structure, the processing, and/or the functioning of the defective CFTR protein.
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