Autosomal dominant polycystic kidney disease results from the loss of the gene product, polycystin 1. Regulatory mechanisms are unresolved, but an apparent G/C sequence bias in the gene is consistent with co-transcriptional R-loop formation. R-loops regulate gene expression and stability, and they form when newly synthesized RNA extensively pairs with the template DNA to displace the non-template strand. In this study, we tested two human sequences for co-transcriptional R-loop formation in vitro. We observed RNase H-sensitive R-loop formation in intron 1 and 22 sequences, but only in one transcriptional orientation. Therefore, R-loops may participate in expression or stability.
Autosomal dominant polycystic kidney disease results from the loss of the gene product, polycystin 1. Regulatory mechanisms are unresolved, but an apparent G/C sequence bias in the gene is consistent with co-transcriptional R-loop formation. R-loops regulate gene expression and stability, and they form when newly synthesized RNA extensively pairs with the template DNA to displace the non-template strand. In this study, we tested two human sequences for co-transcriptional R-loop formation in vitro. We observed RNase H-sensitive R-loop formation in intron 1 and 22 sequences, but only in one transcriptional orientation. Therefore, R-loops may participate in expression or stability.
