A new study has revealed that different combinations of cis-regulatory elements contribute to the chromatin structure of the CFTR gene and to the gene’s varying expression in tissue, according to Lung Disease News. Mutations in the CFTR gene are the sole cause of cystic fibrosis. The complex factors behind the regulatory process of genes are not well understood, and the researchers thought the CFTR gene an appropriate model for gaining a better understanding into them, as indicated on the Lung Disease News report.

Researchers aimed to investigate how cis-regulatory elements contribute to the expression of CFTR in cells from the bronchi, lung, intestine, and male genital duct tract, which are tissues where the CFTR protein is produced in varying amounts. The research team observed that while many other genes have tissue-specific regulatory elements, the CFTR gene uses different combinations of cis-acting elements depending on the tissue type.

The Lung Disease News report notes that, in turn, these combinations engage architectural proteins that fold the chromatin in different ways in the investigated tissues. In the tissues expressing the CFTR gene, the team observed that the chromatin was folded so that the cis-regulatory elements came close to the promoter region, which is the part of a gene initiating transcription.

However, when looking at the CFTR gene in skin fibroblast cells that do not express the CFTR protein, the team noticed that the chromatin was folded in such a way that interactions between the cis-regulatory elements and the promoter were impossible, essentially shutting transcription off.

The authors of the study believe that the results provide new insights into how other genes are regulated. The research study was a collaboration between Rui Yang and colleagues from Lurie Children’s Research Center with Duke University and the Northwestern University Feinberg School of Medicine.

Source: Lung Disease News