The m6A “reader” YTHDF1 promotes osteogenesis of bone marrow mesenchymal stem cells through translational control of ZNF839

The m6A “reader” YTHDF1 promotes osteogenesis of bone marrow mesenchymal stem cells through translational control of ZNF839

Abstract N6-methyladenosine (m6A) is required for differentiation of human bone marrow mesenchymal stem cells (hBMSCs). However, its intrinsic mechanisms are largely unknown. To identify the possible role of m6A binding protein YTHDF1 in hBMSCs osteogenesis in vivo, we constructed Ythdf1 KO mice and...

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Autores principales: Tao Liu, Xinfeng Zheng, Chenglong Wang, Chuandong Wang, Shengdan Jiang, Bo Li, Pengbo Chen, Wenning Xu, Huoliang Zheng, Runze Yang, Xingxu Huang, Xiaoling Zhang, Leisheng Jiang
Formato: article
Lenguaje:EN
Publicado: Nature Publishing Group 2021
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Cytology
QH573-671
Acceso en línea:https://doaj.org/article/3953421029344d2785051f2392b628fb
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spelling oai:doaj.org-article:3953421029344d2785051f2392b628fb2021-11-14T12:06:45ZThe m6A “reader” YTHDF1 promotes osteogenesis of bone marrow mesenchymal stem cells through translational control of ZNF83910.1038/s41419-021-04312-42041-4889https://doaj.org/article/3953421029344d2785051f2392b628fb2021-11-01T00:00:00Zhttps://doi.org/10.1038/s41419-021-04312-4https://doaj.org/toc/2041-4889Abstract N6-methyladenosine (m6A) is required for differentiation of human bone marrow mesenchymal stem cells (hBMSCs). However, its intrinsic mechanisms are largely unknown. To identify the possible role of m6A binding protein YTHDF1 in hBMSCs osteogenesis in vivo, we constructed Ythdf1 KO mice and showed that depletion of Ythdf1 would result in decreased bone mass in vivo. Both deletion of Ythdf1 in mouse BMSCs and shRNA-mediated knockdown of YTHDF1 in hBMSCs prevented osteogenic differentiation of cells in vitro. Using methylated RNA immunoprecipitation (Me-RIP) sequencing and RIP-sequencing, we found that ZNF839 (a zinc finger protein) served as a target of YTHDF1. We also verified its mouse homolog, Zfp839, was translationally regulated by Ythdf1 in an m6A-dependent manner. Zfp839 potentiated BMSC osteogenesis by interacting with and further enhancing the transcription activity of Runx2. These findings should improve our understanding of the mechanism of BMSC osteogenesis regulation and provide new ideas for the prevention and treatment of osteoporosis.Tao LiuXinfeng ZhengChenglong WangChuandong WangShengdan JiangBo LiPengbo ChenWenning XuHuoliang ZhengRunze YangXingxu HuangXiaoling ZhangLeisheng JiangNature Publishing GrouparticleCytologyQH573-671ENCell Death and Disease, Vol 12, Iss 11, Pp 1-13 (2021)
institution DOAJ
collection DOAJ
language EN
topic Cytology
QH573-671
spellingShingle Cytology
QH573-671
Tao Liu
Xinfeng Zheng
Chenglong Wang
Chuandong Wang
Shengdan Jiang
Bo Li
Pengbo Chen
Wenning Xu
Huoliang Zheng
Runze Yang
Xingxu Huang
Xiaoling Zhang
Leisheng Jiang
The m6A “reader” YTHDF1 promotes osteogenesis of bone marrow mesenchymal stem cells through translational control of ZNF839
description Abstract N6-methyladenosine (m6A) is required for differentiation of human bone marrow mesenchymal stem cells (hBMSCs). However, its intrinsic mechanisms are largely unknown. To identify the possible role of m6A binding protein YTHDF1 in hBMSCs osteogenesis in vivo, we constructed Ythdf1 KO mice and showed that depletion of Ythdf1 would result in decreased bone mass in vivo. Both deletion of Ythdf1 in mouse BMSCs and shRNA-mediated knockdown of YTHDF1 in hBMSCs prevented osteogenic differentiation of cells in vitro. Using methylated RNA immunoprecipitation (Me-RIP) sequencing and RIP-sequencing, we found that ZNF839 (a zinc finger protein) served as a target of YTHDF1. We also verified its mouse homolog, Zfp839, was translationally regulated by Ythdf1 in an m6A-dependent manner. Zfp839 potentiated BMSC osteogenesis by interacting with and further enhancing the transcription activity of Runx2. These findings should improve our understanding of the mechanism of BMSC osteogenesis regulation and provide new ideas for the prevention and treatment of osteoporosis.
format article
author Tao Liu
Xinfeng Zheng
Chenglong Wang
Chuandong Wang
Shengdan Jiang
Bo Li
Pengbo Chen
Wenning Xu
Huoliang Zheng
Runze Yang
Xingxu Huang
Xiaoling Zhang
Leisheng Jiang
author_facet Tao Liu
Xinfeng Zheng
Chenglong Wang
Chuandong Wang
Shengdan Jiang
Bo Li
Pengbo Chen
Wenning Xu
Huoliang Zheng
Runze Yang
Xingxu Huang
Xiaoling Zhang
Leisheng Jiang
author_sort Tao Liu
title The m6A “reader” YTHDF1 promotes osteogenesis of bone marrow mesenchymal stem cells through translational control of ZNF839
title_short The m6A “reader” YTHDF1 promotes osteogenesis of bone marrow mesenchymal stem cells through translational control of ZNF839
title_full The m6A “reader” YTHDF1 promotes osteogenesis of bone marrow mesenchymal stem cells through translational control of ZNF839
title_fullStr The m6A “reader” YTHDF1 promotes osteogenesis of bone marrow mesenchymal stem cells through translational control of ZNF839
title_full_unstemmed The m6A “reader” YTHDF1 promotes osteogenesis of bone marrow mesenchymal stem cells through translational control of ZNF839
title_sort m6a “reader” ythdf1 promotes osteogenesis of bone marrow mesenchymal stem cells through translational control of znf839
publisher Nature Publishing Group
publishDate 2021
url https://doaj.org/article/3953421029344d2785051f2392b628fb
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