Molecular basis of multifunctional expression induced by the mRNA splicing selective in undifferentiated epithelium

2017 Fiscal Year Final Research Report

• Project/Area Number: 26670104
• Research Category: Grant-in-Aid for Challenging Exploratory Research
• Allocation Type: Multi-year Fund
• Research Field: General physiology
• Research Institution: Fukuoka Dental College
• Principal Investigator: Yamazaki Jun 福岡歯科大学, 口腔歯学部, 教授 (50230397)
• Co-Investigator(Kenkyū-buntansha): 八田 光世 福岡歯科大学, 口腔歯学部, 准教授 (30344518) ; 岡村 和彦 福岡歯科大学, 口腔歯学部, 准教授 (00224056)
• Research Collaborator: KATO Kenichi 福岡歯科大学, 口腔歯学部, 非常勤講師 (90320332)
• Project Period (FY): 2014-04-01 – 2018-03-31
• Keywords: スプライシング / 上皮細胞 / クロライドチャネル / 分化 / エピジェネティックス

Outline of Final Research Achievements

This project aims to clarify the mRNA splicing mechanism in which Ca2+-activated Cl- channel modulator CLCA is switched to its truncated isoform (CLCA-t). Using the splicing reporter plasmids including the gene region (minigene) of exons 8, 9 and 10, the splicing pattern of which is distinct between two CLCA isoforms, the splicing pattern observed in CLCA-t (exon 8+10) was shown to be attenuated by the differentiation of epithelium. Next, we examined the epigenetic regulation of the selective splicing of CLCA in the 3-dimensional mucosal culture model. Overall, trimethylation of histone that reportedly alters the chromatin structure is likely to contribute to the splicing pattern in the CLCA isoforms.

Free Research Field

薬理学