MicroRNA-142 controls thymocyte proliferation

Alexander Mildner, Elik Chapnik, Diana Varol, Tegest Aychek, Nardi Lampl, Natalia Rivkin, Anita Bringmann, Franziska Paul, Sigalit Boura-Halfon, Yifat Segal Hayoun, Zohar Barnett-Itzhaki, Ido Amit, Eran Hornstein*, Steffen Jung

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

29 Scopus citations

Abstract

T-cell development is a spatially and temporally regulated process, orchestrated by well-defined contributions of transcription factors and cytokines. Here, we identify the noncoding RNA miR-142 as an additional regulatory layer within murine thymocyte development and proliferation. MiR-142 deficiency impairs the expression of cell cycle-promoting genes in mature mouse thymocytes and early progenitors, accompanied with increased levels of cyclin-dependent kinase inhibitor 1B (Cdkn1b, also known as p27Kip1). By using CRISPR/Cas9 technology to delete the miR-142-3p recognition element in the 3’UTR of cdkn1b, we confirm that this gene is a novel target of miR-142-3p in vivo. Increased Cdkn1b protein expression alone however was insufficient to cause proliferation defects in thymocytes, indicating the existence of additional critical miR-142 targets. Collectively, we establish a key role for miR-142 in the control of early and mature thymocyte proliferation, demonstrating the multifaceted role of a single miRNA on several target genes.

Original languageAmerican English
Pages (from-to)1142-1152
Number of pages11
JournalEuropean Journal of Immunology
Volume47
Issue number7
DOIs
StatePublished - Jul 2017
Externally publishedYes

Bibliographical note

Publisher Copyright:
© 2017 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim

Keywords

  • Posttranscriptional control
  • Thymocyte development
  • microRNAs

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