BCAS2 supplementary information
Insulin secreted by pancreatic β cells is essential for maintaining the level of blood glucose. Diabetes is caused primarily by loss of β cells or impairment of β cell function. A previous whole-transcriptome analysis of islets from a type 2 diabetes (T2D) group and a control group showed that splicing disorder occurred in approximately 25% of splicing events. Breast carcinoma amplified sequence 2 (BCAS2) is a spliceosome component whose function in islet β cells is unclear. Here, we report that knockdown of Bcas2 decreased glucose- and KCl-stimulated insulin secretion in the NIT-1 cell line. Pancreas weight, glucose tolerance and insulin sensitivity were measured in normal chow-fed Bcas2 f/f-βKO mice, and β cell mass and islet size were analyzed by immunohistochemistry. Glucose intolerance developed in Bcas2 f/f-βKO mice, but there were no significant differences in pancreas weight, insulin sensitivity, β cell mass or islet size. Furthermore, observation of glucose-stimulated insulin secretion (GSIS) and insulin secretion granules in normal chow-fed mice revealed that the insulin level in serum and the number of insulin secretion granules were decreased in Bcas2 f/f-βKO mice. These differences were related to abnormal splicing of Syt7 and Tcf7l2 pre-mRNA. Taken together, these results demonstrate that BCAS2 is involved in alternative splicing during insulin synthesis and secretion. The data is supplementary to"BCAS2 participates in insulin synthesis and secretion via mRNA alternative splicing in mice".