Analyses of molecular mechanism of small intestine epithelia formation

2014 Fiscal Year Final Research Report

• Project/Area Number: 24659084
• Research Category: Grant-in-Aid for Challenging Exploratory Research
• Allocation Type: Multi-year Fund
• Research Field: General anatomy (including Histology/Embryology)
• Research Institution: Osaka University
• Principal Investigator: HARADA Akihiro 大阪大学, 医学(系)研究科(研究院), 教授 (40251441)
• Co-Investigator(Kenkyū-buntansha): KUNII Masataka 大阪大学, 大学院医学系研究科, 助教 (80614768)
• Project Period (FY): 2012-04-01 – 2015-03-31
• Keywords: 細胞極性 / SNARE

Outline of Final Research Achievements

Deficiency in syntaxin3, known to be important in apical transport, caused defects in apical transport and cell proliferation in polarized cells. To know the molecular mechanism of these phenotype, we generated an apical marker protein which is expressed after drug administration. As the marker worked well in cell lines, we induced the gene into primary cultured cells and we will look at the transport after getting sufficient amount of cells. To make model system to examine the molecular mechanism, we introduced Cre recombinase into primary cultured cells and we are expanding the cells now. In addition, we successfully generated intestinal cell lines which lacks syntaxin3 by CRISPR method. As we observed similar phenotype in these cell lines, we are planning to use these cells for elucidation of molecular mechanism of apical transport and cell proliferation.

Free Research Field

細胞生物学