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核心结合因子 CBF 负调控骨骼肌终末分化。

The core binding factor CBF negatively regulates skeletal muscle terminal differentiation.

机构信息

Institut André Lwoff, FRE2944, CNRS and Université Paris-Sud, Villejuif, France.

出版信息

PLoS One. 2010 Feb 25;5(2):e9425. doi: 10.1371/journal.pone.0009425.

DOI:10.1371/journal.pone.0009425
PMID:20195544
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2828485/
Abstract

BACKGROUND

Core Binding Factor or CBF is a transcription factor composed of two subunits, Runx1/AML-1 and CBF beta or CBFbeta. CBF was originally described as a regulator of hematopoiesis.

METHODOLOGY/PRINCIPAL FINDINGS: Here we show that CBF is involved in the control of skeletal muscle terminal differentiation. Indeed, downregulation of either Runx1 or CBFbeta protein level accelerates cell cycle exit and muscle terminal differentiation. Conversely, overexpression of CBFbeta in myoblasts slows terminal differentiation. CBF interacts directly with the master myogenic transcription factor MyoD, preferentially in proliferating myoblasts, via Runx1 subunit. In addition, we show a preferential recruitment of Runx1 protein to MyoD target genes in proliferating myoblasts. The MyoD/CBF complex contains several chromatin modifying enzymes that inhibits MyoD activity, such as HDACs, Suv39h1 and HP1beta. When overexpressed, CBFbeta induced an inhibition of activating histone modification marks concomitant with an increase in repressive modifications at MyoD target promoters.

CONCLUSIONS/SIGNIFICANCE: Taken together, our data show a new role for Runx1/CBFbeta in the control of the proliferation/differentiation in skeletal myoblasts.

摘要

背景

核心结合因子或 CBF 是由两个亚基组成的转录因子，Runx1/AML-1 和 CBFβ或 CBFbeta。CBF 最初被描述为造血的调节剂。

方法/主要发现：在这里，我们表明 CBF 参与控制骨骼肌终末分化。事实上，下调 Runx1 或 CBFbeta 蛋白水平会加速细胞周期退出和肌肉终末分化。相反，CBFβ在成肌细胞中的过表达会减缓终末分化。CBF 通过 Runx1 亚基与主肌生成转录因子 MyoD 直接相互作用，优先在增殖的成肌细胞中。此外，我们还显示 Runx1 蛋白优先招募到增殖的成肌细胞中的 MyoD 靶基因。MyoD/CBF 复合物包含几种抑制 MyoD 活性的染色质修饰酶，如 HDACs、Suv39h1 和 HP1beta。当过表达时，CBFβ 诱导激活组蛋白修饰标记的抑制，同时在 MyoD 靶启动子上增加抑制修饰。

结论/意义：总之，我们的数据显示 Runx1/CBFβ在控制骨骼肌成肌细胞增殖/分化方面具有新的作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f0c2/2828485/333642e43f89/pone.0009425.g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f0c2/2828485/b083981ae3bd/pone.0009425.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f0c2/2828485/9974268d720a/pone.0009425.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f0c2/2828485/306f43a20e43/pone.0009425.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f0c2/2828485/b26eb56dcc44/pone.0009425.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f0c2/2828485/86dd9bb12d17/pone.0009425.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f0c2/2828485/333642e43f89/pone.0009425.g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f0c2/2828485/b083981ae3bd/pone.0009425.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f0c2/2828485/9974268d720a/pone.0009425.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f0c2/2828485/306f43a20e43/pone.0009425.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f0c2/2828485/b26eb56dcc44/pone.0009425.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f0c2/2828485/86dd9bb12d17/pone.0009425.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f0c2/2828485/333642e43f89/pone.0009425.g006.jpg

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