[PhD Thesis Public Presentation_C700, Lab3_Zoom is also available] ‐ Hsiao-Chiao Chien- "JunB is Essential for Chromatin Regulation in Pathogenic Th17 Cells"


Wednesday, February 14, 2024 - 16:00 to 17:00


C700, Lab3 Level C ( Zoom is also available)


Presenter: Hsiao-Chiao Chien

Supervisor: Prof. Hiroki Ishikawa

Unit: Immune Signal Unit




Title: JunB is Essential for Chromatin Regulation in Pathogenic Th17 Cells



Epigenetic regulation and chromatin remodeling play critical role in governing gene expression during T helper (Th) cell differentiation. JunB, a member of the AP-1 transcription factor family, is required for autoimmune pathogenic Th17 transcriptional program, but its role in the chromatin regulation remains unknown. Using the assay for transposase-accessible chromatin sequencing (ATAC-seq), I found that JunB regulates chromatin remodeling in differentiation of diverse T helper subsets in vivo and in vitro. Particularly, in pathogenic Th17 differentiation, JunB promotes chromatin accessibility at enhancer regions associated with a subset of Th17-related genes, including interleukin 17a (Il17a) and Il23 receptor (Il23r). JunB is necessary for BATF pioneering functions and/or the deposition of histone modifications, H3K4me1 and H3K27ac, through the recruitment of histone methyltransferase MLL4, and the recruitment of the BAF chromatin remodeling complex at these loci. Moreover, JunB indirectly inhibits chromatin accessibility at loci related to fate switch from Th17 to Th1 cells, such as interferon gamma (Ifng), likely through inhibiting chromatin accessibility and expression of an immediate-early transcription factors, such as NF-kB, NR4A1, Ets and Runx family members. These results indicate that JunB is essential for enhancer activation of Th17-related genes, while indirectly inhibiting chromatin accessibility in diverse regions regulated by other key transcription factors.

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