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February 8, 2026eLife0 citationsOpen Access

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

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YMYuji MiyatakeTKTakeshi KamakuraRYRyo Yanagiya

Key Points

  • This research aims to investigate the role of miR-195 in B cell development, particularly when EBF1 is deficient.
  • Transduction of miR-195 into EBF1-deficient hematopoietic progenitor cells
  • Assessment of CD19 expression and V(D)J recombination
  • Analysis of FOXO1 accumulation and phosphorylation pathways
  • EBF1-deficient progenitor cells expressing miR-195 successfully showed CD19 expression
  • V(D)J recombination and class switch recombination occurred without EBF1
  • FOXO1 accumulation was linked to inhibited phosphorylation pathways impacted by miR-195

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 ( 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.

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Cite This Study

Miyatake et al. (2026) studied this question.

synapsesocial.com/papers/698828010fc35cd7a8847150https://doi.org/10.7554/elife.101510.3
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