The meiotic TERB1-TERB2-MAJIN complex tethers telomeres to the nuclear envelope

Nat Commun. 2019 Feb 4;10(1):564. doi: 10.1038/s41467-019-08437-1.

Yan Wang ¹, Yanyan Chen ¹, Juan Chen ² ³, Lijun Wang ¹, Leitong Nie ⁴, Juanjuan Long ¹, Haishuang Chang ² ³, Jian Wu ² ³, Chenhui Huang ⁵ ⁶, Ming Lei ⁷ ⁸ ⁹

Affiliations

1 National Center for Protein Science Shanghai, State Key Laboratory of Molecular Biology, CAS Center for Excellence on Molecular Cell Science, Institute of Biochemistry and Cell Biology, Chinese Academy of Sciences, University of Chinese Academy of Sciences, 200031, Shanghai, China.
2 Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, 200011, Shanghai, China.
3 Shanghai Institute of Precision Medicine, 200125, Shanghai, China.
4 National Key Laboratory of Crop Genetic Improvement, Huazhong Agriculture University, 430072, Wuhan, China.
5 Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, 200011, Shanghai, China. huangchh@shsmu.edu.cn.
6 Shanghai Institute of Precision Medicine, 200125, Shanghai, China. huangchh@shsmu.edu.cn.
7 Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, 200011, Shanghai, China. leim@shsmu.edu.cn.
8 Shanghai Institute of Precision Medicine, 200125, Shanghai, China. leim@shsmu.edu.cn.
9 Key laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Shanghai Jiao Tong University School of Medicine, 200025, Shanghai, China. leim@shsmu.edu.cn.

PMID: 30718482 DOI: 10.1038/s41467-019-08437-1

Abstract

During meiotic prophase I, telomeres attach to and move on the nuclear envelope (NE), regulating chromosome movement to promote homologous pairing. Meiosis-specific proteins TERB1, TERB2 and MAJIN play a key role in this process. Here, we report the crystal structures of human TERB1-TERB2 and TERB2-MAJIN subcomplexes. Specific disruption of the TERB1-TERB2 or the TERB2-MAJIN interaction in the mouse Terb2 gene abolishes the telomere attachment to the NE and causes aberrant homologous pairing and disordered synapsis. In addition, depletion of SUN1 also partially disrupts the telomere-NE connection. We propose that the telomere-TRF1-TERB1-TERB2-MAJIN-NE interaction network and the telomere-LINC complex connection are likely two separate but cooperative pathways to stably recruit telomeres to the NE in meiosis prophase I. Our work provides a molecular model of the connection between telomeres and the NE and reveals the correlation between aberrant synapsis and the defective telomere attachment to the NE.

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