Loss of MBD2 affects early T cell development by inhibiting the WNT signaling pathway.

Ling Cheng, Kuangguo Zhou, Xing Chen, Jing Zhou, Wei Cai, Yingchi Zhang, Xiaomin Wang, Congyi Wang, Weiping Yuan, Jianfeng Zhou, Mi Zhou

Experimental cell research 2021 Jan 01

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DNA methylation alters the expression of certain genes without any alteration to the DNA sequence and is a dynamic process during normal hematopoietic differentiation. As an epigenetic regulator, methyl-CpG-binding domain protein 2 (MBD2) is an important member of the MBD protein family and is acknowledged as a "reader" of DNA methylation. We used a mouse model to study the effects of MBD2 on the early development of T cells. Here, we found that MBD2 deficiency led to retardation of T cell differentiation at the DN3 stage. Meanwhile, decreased proliferative capacity and increased apoptosis were detected in Mbd2-/- DN thymocytes. Furthermore, we found the WNT pathway was significantly down-regulated in Mbd2-/- DN thymocytes: DKK1 (Dickkopf-1) expression was significantly increased, while TCF7 (transcription factor 7) and c-MYC were down-regulated. Thus, these findings established that MBD2 acted as a dominant regulator to imprint DN T cell development via the WNT pathway. Copyright © 2020 Elsevier Inc. All rights reserved.

Citation

Ling Cheng, Kuangguo Zhou, Xing Chen, Jing Zhou, Wei Cai, Yingchi Zhang, Xiaomin Wang, Congyi Wang, Weiping Yuan, Jianfeng Zhou, Mi Zhou. Loss of MBD2 affects early T cell development by inhibiting the WNT signaling pathway. Experimental cell research. 2021 Jan 01;398(1):112400