miR-195 Enables EBF1-Independent B Cell Differentiation via FOXO1 Accumulation (Kotani Lab, in eLife)

Accumulated studies have reported that hematopoietic differentiation was primarily regulated by transcription factors. Early B cell factor 1 (EBF1) is an essential transcription factor for B lymphopoiesis. Contrary to the canonical notion, we found that a single miRNA, miRNA-195 (Mir195) transduction let Ebf1-deficient hematopoietic progenitor cells (HPCs) express CD19, carry out V(D)J recombination and class switch recombination, which implied that B cell matured without EBF1. A part of the mechanism was caused by FOXO1 accumulation via inhibition of FOXO1 phosphorylation pathways in which targets of Mir195 are enriched. These results suggested that some miRNA transductions could function as alternatives to transcription factors.

 

This Article was published in eLiFE, February 2026.

Title: A single microRNA miR-195 rescues the arrested B cell development induced by EBF1 deficiency

Authors: Yuji Miyatake, Takeshi Kamakura, Tomokatsu Ikawa, Ryo Yanagiya, Ryutaro Kotaki, Kazuaki Kameda, Ryo Koyama-Nasu, Kazuki Okuyama, Ken-ichi Hirano, Hiroyuki Hosokawa, Katsuto Hozumi, Masato Ohtsuka, Takahiro Kishikawa, Chikako Shibata, Motoyuki Otsuka, Reo Maruyama, Kiyoshi Ando, Tomohiro Kurosaki, Hiroshi Kawamoto, Ai Kotani

Doi: 10.7554/eLife.101510.2

  • Fig) Graphical abstract. Mir195 induced CD19 expression without EBF1, suggesting that Mir195 compensated for EBF1 deficiency in B cell development.