2020 Vol. 11, No. 12

TRIM35, TRAF3, and PB2 of influenza A virus (IAV) form a circuit in which two means are employed by TRIM35 to defend the host against IAV infection. TRIM35 is a positive regulator of RIG-I-mediated innate immunity, leading to enhanced production of type I interferon by facilitating K63-linked polyubiquitination of TRAF3. Although IAV PB2 prevents K63-linked polyubiquitination of TRAF3, TRIM35 directly mediates K48-linked polyubiquitination and degradation of IAV PB2.

Tso-Hsin Cheng: The founder of modern ornithology and zoogeography in China
Fumin Lei, Gang Song
2020, 11(12): 859-861. doi: 10.1007/s13238-020-00761-3
First progeria monkey model generated using base editor
Pradeep Reddy, Yanjiao Shao, Reyna Hernandez-Benitez, Estrella Nuñez Delicado, Juan Carlos Izpisua Belmonte
2020, 11(12): 862-865. doi: 10.1007/s13238-020-00765-z
New avenues for systematically inferring cellcell communication: through single-cell transcriptomics data
Xin Shao, Xiaoyan Lu, Jie Liao, Huajun Chen, Xiaohui Fan
2020, 11(12): 866-880. doi: 10.1007/s13238-020-00727-5
For multicellular organisms, cell-cell communication is essential to numerous biological processes. Drawing upon the latest development of single-cell RNA-sequencing (scRNA-seq), high-resolution transcriptomic data have deepened our understanding of cellular phenotype heterogeneity and composition of complex tissues, which enables systematic cell-cell communication studies at a single-cell level. We first summarize a common workflow of cell-cell communication study using scRNA-seq data, which often includes data preparation, construction of communication networks, and result validation. Two common strategies taken to uncover cell-cell communications are reviewed, e.g., physically vicinal structure-based and ligand-receptor interaction-based one. To conclude, challenges and current applications of cell-cell communication studies at a single-cell resolution are discussed in details and future perspectives are proposed.
How are MCPIP1 and cytokines mutually regulated in cancer-related immunity?
Ruyi Xu, Yi Li, Yang Liu, Jianwei Qu, Wen Cao, Enfan Zhang, Jingsong He, Zhen Cai
2020, 11(12): 881-893. doi: 10.1007/s13238-020-00739-1
Cytokines are secreted by various cell types and act as critical mediators in many physiological processes, including immune response and tumor progression. Cytokines production is precisely and timely regulated by multiple mechanisms at different levels, ranging from transcriptional to post-transcriptional and posttranslational processes. Monocyte chemoattractant protein-1 induced protein 1 (MCPIP1), a potent immunosuppressive protein, was first described as a transcription factor in monocytes treated with monocyte chemoattractant protein-1 (MCP-1) and subsequently found to possess intrinsic RNase and deubiquitinase activities. MCPIP1 tightly regulates cytokines expression via various functions. Furthermore, cytokines such as interleukin 1 beta (IL-1B) and MCP-1 and inflammatory cytokines inducer lipopolysaccharide (LPS) strongly induce MCPIP1 expression. Mutually regulated MCPIP1 and cytokines form a complicated network in the tumor environment. In this review, we summarize how MCPIP1 and cytokines reciprocally interact and elucidate the effect of the network formed by these components in cancer-related immunity with aim of exploring potential clinical benefits of their mutual regulation.
Research article
TRIM35 mediates protection against influenza infection by activating TRAF3 and degrading viral PB2
Nan Sun, Li Jiang, Miaomiao Ye, Yihan Wang, Guangwen Wang, Xiaopeng Wan, Yuhui Zhao, Xia Wen, Libin Liang, Shujie Ma, Liling Liu, Zhigao Bu, Hualan Chen, Chengjun Li
2020, 11(12): 894-914. doi: 10.1007/s13238-020-00734-6
Tripartite motif (TRIM) family proteins are important effectors of innate immunity against viral infections. Here we identified TRIM35 as a regulator of TRAF3 activation. Deficiency in or inhibition of TRIM35 suppressed the production of type I interferon (IFN) in response to viral infection. Trim35-deficient mice were more susceptible to influenza A virus (IAV) infection than were wild-type mice. TRIM35 promoted the RIG-Imediated signaling by catalyzing Lys63-linked polyubiquitination of TRAF3 and the subsequent formation of a signaling complex with VISA and TBK1. IAV PB2 polymerase countered the innate antiviral immune response by impeding the Lys63-linked polyubiquitination and activation of TRAF3. TRIM35 mediated Lys48-linked polyubiquitination and proteasomal degradation of IAV PB2, thereby antagonizing its suppression of TRAF3 activation. Our in vitro and in vivo findings thus reveal novel roles of TRIM35, through catalyzing Lys63-or Lys48-linked polyubiquitination, in RIG-I antiviral immunity and mechanism of defense against IAV infection.
Rewiring ERBB3 and ERK signaling confers resistance to FGFR1 inhibition in gastrointestinal cancer harbored an ERBB3-E928G mutation
Xiang Yang, Hongxiao Wang, Enjun Xie, Biyao Tang, Qingdian Mu, Zijun Song, Junyi Chen, Fudi Wang, Junxia Min
2020, 11(12): 915-920. doi: 10.1007/s13238-020-00749-z
Biallelic mutations in CDC20 cause female infertility characterized by abnormalities in oocyte maturation and early embryonic development
Lin Zhao, Songguo Xue, Zhongyuan Yao, Juanzi Shi, Biaobang Chen, Ling Wu, Lihua Sun, Yao Xu, Zheng Yan, Bin Li, Xiaoyan Mao, Jing Fu, Zhihua Zhang, Jian Mu, Wenjing Wang, Jing Du, Shuai Liu, Jie Dong, Weijie Wang, Qiaoli Li, Lin He, Li Jin, Xiaozhen Liang, Yanping Kuang, Xiaoxi Sun, Lei Wang, Qing Sang
2020, 11(12): 921-927. doi: 10.1007/s13238-020-00756-0
Correction to: Characterization of oogonia stem cells in mice by Fragilis
Xiaoyan Sheng, Chenglei Tian, Linlin Liu, Lingling Wang, Xiaoying Ye, Jie Li, Ming Zeng, Lin Liu
2020, 11(12): 928-930. doi: 10.1007/s13238-020-00743-5