TANGO6 regulates cell proliferation via COPI vesicle-mediated RPB2 nuclear entry

Zhi Feng, Shengnan Liu, Ming Su, Chunyu Song, Chenyu Lin, Fangying Zhao, Yang Li, Xianyan Zeng, Yong Zhu, Yu Hou, Chunguang Ren, Huan Zhang, Ping Yi, Yong Ji, Chao Wang, Hongtao Li, Ming Ma, Lingfei Luo () and Li Li ()
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Zhi Feng: Chinese Academy of Sciences
Shengnan Liu: Southwest University
Ming Su: Chinese Academy of Sciences
Chunyu Song: Southwest University
Chenyu Lin: Southwest University
Fangying Zhao: Southwest University
Yang Li: Chinese Academy of Sciences
Xianyan Zeng: Chongqing Medical University
Yong Zhu: Chongqing Medical University
Yu Hou: Chongqing Medical University
Chunguang Ren: Chongqing Medical University
Huan Zhang: Chongqing Medical University
Ping Yi: The Third Affiliated Hospital of Chongqing Medical University
Yong Ji: Nanjing Medical University
Chao Wang: University of Science and Technology of China
Hongtao Li: Southwest University
Ming Ma: Southwest University
Lingfei Luo: Southwest University
Li Li: Chinese Academy of Sciences

Nature Communications, 2024, vol. 15, issue 1, 1-17

Abstract: Abstract Coat protein complex I (COPI) vesicles mediate the retrograde transfer of cargo between Golgi cisternae and from the Golgi to the endoplasmic reticulum (ER). However, their roles in the cell cycle and proliferation are unclear. This study shows that TANGO6 associates with COPI vesicles via two transmembrane domains. The TANGO6 N- and C-terminal cytoplasmic fragments capture RNA polymerase II subunit B (RPB) 2 in the cis-Golgi during the G1 phase. COPI-docked TANGO6 carries RPB2 to the ER and then to the nucleus. Functional disruption of TANGO6 hinders the nuclear entry of RPB2, which accumulates in the cytoplasm, causing cell cycle arrest in the G1 phase. The conditional depletion or overexpression of TANGO6 in mouse hematopoietic stem cells results in compromised or expanded hematopoiesis. Our study results demonstrate that COPI vesicle-associated TANGO6 plays a role in the regulation of cell cycle progression by directing the nuclear transfer of RPB2, making it a potential target for promoting or arresting cell expansion.

Date: 2024
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DOI: 10.1038/s41467-024-46720-y

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