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

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; T. Kishikawa; Chikako Shibata; Motoyuki Otsuka; Reo Maruyama; Kiyoshi Ando; Tomohiro Kurosaki; Hiroshi Kawamoto; Ai Kotani

doi:10.7554/elife.101510.3

ImmunologyeLifeJan 28, 2026

Peer-reviewed journal article

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

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

Abstract

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 (miR-195) 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 miR-195 are enriched. These results suggested that some miRNA transductions could function as alternatives to transcription factors.

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