Elucidation of molecular mechanism of function of long noncoding RNAs through methylation signal

2015 Fiscal Year Final Research Report

• Project/Area Number: 25293073
• Research Category: Grant-in-Aid for Scientific Research (B)
• Allocation Type: Partial Multi-year Fund
• Section: 一般
• Research Field: General medical chemistry
• Research Institution: Saitama Medical University
• Principal Investigator: KUROKAWA RIKI 埼玉医科大学, 医学部, 教授 (70170107)
• Co-Investigator(Kenkyū-buntansha): FUJIMOTO KENTA 埼玉医科大学, 医学部, 助教 (50403580)
• Co-Investigator(Renkei-kenkyūsha): MATSUSITA AKIO 埼玉医科大学, 医学部, 客員講師 (50402269) ; OGAWA SUMITO 東京大学, 医学部附属病院, 准教授 (20323579)
• Project Period (FY): 2013-04-01 – 2016-03-31
• Keywords: 酵素 / 遺伝子 / 核酸 / 生体分子 / 発現制御 / メチル化 / 長鎖非コードRNA

Outline of Final Research Achievements

We have demonstrated that the promoter-associated noncoding RNA-D (pncRNA-D) transcribed from a promoter region of the cyclin D1 gene represses its expression through binding of pncRNA-D to RNA-binding protein TLS (Nature 454: 126-130, 2008). TLS is found to target the 5’ end (32-62) of pncRNA-D. At the 3’ end (44-62) of pncRNA-D forms a stem-loop structure, while TLS firmly binds to the straight chain of the 5’ end (32-44) of pncRNA. Moreover, high-osmotic treatment of HeLa cells reduced methylation of the N6-adenosine (m6A) at pncRNA-D, but induced its binding to TLS. Recently, we have been analyzing effect of methylation of TLS on its binding to pncRNA-D. Methylation of long ncRNAs (lncRNAs) might regulate their physiological function presenting another exciting issue of the lncRNA biology.

Free Research Field

基礎医学・医科学一般