Analysis of the chromatin status in an ultra-low scale

2017 Fiscal Year Final Research Report

• Project/Area Number: 15K21113
• Research Category: Grant-in-Aid for Young Scientists (B)
• Allocation Type: Multi-year Fund
• Research Field: Tumor biology; Human genetics
• Research Institution: Kyoto University
• Principal Investigator: Tanaka Azusa 京都大学, 医学研究科, 特別研究員(PD) (70749796)
• Project Period (FY): 2015-04-01 – 2018-03-31
• Keywords: エピゲノム / 細胞分化 / 成人T細胞白血病 / クロマチン

Outline of Final Research Achievements

It is now accepted that the initiation and progression of cancer, traditionally seen as a genetic disease, also involves epigenetic aberrations. Human T-cell leukemia virus type 1 (HTLV-1) is an oncogenic retrovirus and the etiological agent of adult T-cell leukemia-lymphoma (ATL). Here, we performed ATAC-seq on ATL cell samples and discovered global alterations in the chromatin status. For this experiment, we modified original ATAC-seq protocol to apply this method to limited number of cells in clinical samples. To characterize differences in chromatin accessibility in ATL cells and normal human CD4+ memory T cells, we searched for regions of gained and lost genome accessibility. Motif analysis of increased accessible sites in ATL cells identified a strong enrichment in bZIP family transcription factors. Now we are performing a knock down experiment to confirm the importance of this transcription factor.

Free Research Field

エピゲノム