BCAS2 Participates in Insulin Synthesis and Secretion via mRNA Alternative Splicing in Mice

Author:

Chen Xuexue1,Xie Xiaomei1,Li Jianhua2,Sun Longjie1ORCID,Lv Zheng1,Yao Xiaohong1,Li Lei3,Jin Hua4ORCID,Cui Sheng5ORCID,Liu Jiali1ORCID

Affiliation:

1. State Key Laboratory of Animal Biotech Breeding, College of Biological Sciences, China Agricultural University , Beijing 100193 , China

2. Reproductive Medical Center, Department of Obstetrics and Gynecology, the Seventh Medical Center of PLA General Hospital , Beijing 100007 , China

3. State Key Laboratory of Stem Cell and Reproductive Biology, Institute of Zoology, Chinese Academy of Sciences , Beijing 100101 , China

4. Department of Pathology, the Seventh Medical Center of PLA General Hospital , Beijing 100007 , China

5. College of Veterinary Medicine, Yangzhou University , Yangzhou, Jiangsu 225009 , China

Abstract

Abstract Insulin secreted by pancreatic β cells is essential for maintaining blood glucose levels. Diabetes is caused primarily by a loss of β cells or impairment of β-cell function. A previous whole-transcriptome analysis of islets from a type 2 diabetes group and a control group showed that a 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 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.

Funder

National Key Research & Developmental Program of China

National Natural Science Foundation of China

Beijing Natural Science Foundation

China Agricultural University

Publisher

The Endocrine Society

Subject

Endocrinology

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