DCAF1 controls T-cell function via p53-dependent and -independent mechanisms

Zengli Guo, Qing Kong, Cui Liu, Song Zhang, Liyun Zou, Feng Yan, Jason K. Whitmire, Yue Xiong, Xian Chen and Yisong Y. Wan ()
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Zengli Guo: Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill
Qing Kong: Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill
Cui Liu: Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill
Song Zhang: Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill
Liyun Zou: Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill
Feng Yan: Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill
Jason K. Whitmire: University of North Carolina at Chapel Hill
Yue Xiong: Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill
Xian Chen: Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill
Yisong Y. Wan: Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill

Nature Communications, 2016, vol. 7, issue 1, 1-13

Abstract: Abstract On activation, naive T cells grow in size and enter cell cycle to mount immune response. How the fundamental processes of T-cell growth and cell cycle entry are regulated is poorly understood. Here we report that DCAF1 (Ddb1–cullin4-associated-factor 1) is essential for these processes. The deletion of DCAF1 in T cells impairs their peripheral homeostasis. DCAF1 is upregulated on T-cell receptor activation and critical for activation-induced T-cell growth, cell cycle entry and proliferation. In addition, DCAF1 is required for T-cell expansion and function during anti-viral and autoimmune responses in vivo. DCAF1 deletion leads to a drastic stabilization of p53 protein, which can be attributed to a requirement of DCAF1 for MDM2-mediated p53 poly-ubiquitination. Importantly, p53 deletion rescues the cell cycle entry defect but not the growth defect of DCAF1-deficient cells. Therefore, DCAF1 is vital for T-cell function through p53-dependent and -independent mechanisms.

Date: 2016
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DOI: 10.1038/ncomms10307

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