Published online Mar 15, 2019. doi: 10.4239/wjd.v10.i3.181
Peer-review started: February 10, 2019
First decision: February 19, 2019
Revised: March 8, 2019
Accepted: March 11, 2019
Article in press: March 11, 2019
Published online: March 15, 2019
Processing time: 37 Days and 20.3 Hours
Diabetes mellitus is a global health challenge, which is usually associated with the loss/dysfunction of insulin-producing pancreatic beta cells. Hence, understanding the molecular mechanisms that control beta cells differentiation and function represents a major interest in the medical field. Regulatory factor X6 (RFX6) is DNA binding protein that is predominantly expressed in pancreatic islets of human and plays a key role in regulating pancreatic beta cells differentiation and insulin production, and it has been recently. RFX6 contains a highly conserved DNA binding domain which is critical for binding of RFX6 to DNA and consequently regulates the amount of messenger RNA produced by the gene. Several lines of evidence have indicated that RFX6 binding to DNA could be disrupted in diabetes. However, the mechanism by which this could happen is still unknown.
The presence of genetic mutations in the gene coding for the RFX6-DNA binding domain could result in inhibition of binding of RFX6 to DNA and consequently loss of function. Defining such genetic mutations will provide valuable information to diagnose, treat, prevent and cure type 2 diabetes (T2D).
In this study, we sought to investigate if any structural genetic mutations could be present in the RFX6-DNA binding domain in T2D patients and whether they are associated with diabetes.
A case-control study was conducted in T2D patients and healthy volunteers. The DNA was extracted from all subjects and polymerase chain reaction (PCR) was used to amplify genomic DNA encompassing the coding sequences and intronic borders of exons 3, 4, 5 and 6 of the RFX6 gene, then PCR samples were analysed by DNA sequencing.
Our data showed the absence of any mutation in the exons coding for the RFX6-DNA binding domain. However, we have identified a new heterozygous single nucleotide polymorphism (IVS6+31 C>T) in the intronic region of DNA binding domain gene that is present in 9.2% and 8.5% of diabetic and control people, respectively (P = 0.97).
We conclude that genetic mutations in the DNA binding domain of RFX6 are unlikely to exist in T2D.
RFX6 binding to DNA is mediated by multiple of domains. Indeed, RFX6 proteins contain other conserved regions, including B, C, and D domains, which play a critical role in oligomerization of the protein and are required for DNA binding and activation. Thus, testing the other functional domains of RFX6 in future will provide more insights into the role of RFX6 in diabetes.