简介

作为国际上最有影响力之一的科技出版社，总部设在美国剑桥市的细胞出版社（Cell Press）一直致力于推动科技创新和科学信息的传播交流。细胞出版社成立于1986年，并于1998年加入爱思唯尔出版集团。细胞出版社目前出版发行包括Cell系列、Trends综述系列等在内的超过三十种期刊，并与世界上多家学会共同合作办刊，覆盖了从细胞和分子生物学到转化及临床医学研究到化学等广泛领域的最新发现及动态。

华人学者研究亮点

封面文章：Dlk2-Gtl2基因座对造血干细胞的影响

The Dlk1-Gtl2 Locus Preserves LT-HSC Function by Inhibiting the PI3K-mTOR Pathway to Restrict Mitochondrial Metabolism

Article

Pengxu Qian, Xi C. He, Ariel Paulson, Zhenrui Li, Fang Tao, John M. Perry, Fengli Guo, Meng Zhao, Lei Zhi, Aparna Venkatraman, Jeffrey S. Haug, Tari Parmely, Hua Li, Rick T. Dobrowsky, Wen-Xing Ding, Tomohiro Kono, Anne C. Ferguson-Smith, Linheng Li

DOI: http://dx.doi.org/10.1016/j.stem.2015.11.001

Cell Stem Cell, Vol. 18, Issue 2, p214–228

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xQian and colleagues show that ncRNAs expressed from the imprinted locus Dlk1-Gtl2 maintain fetal liver and adult LT-HSCs through multiplexed inhibition of PI3K-mTOR signaling that in turn keeps mitochondrial biogenesis and metabolic activity in check.

封面文章：化学诱导重编程产生多功能干细胞过程的一个中间状态

A XEN-like State Bridges Somatic Cells to Pluripotency during Chemical Reprogramming

Article

Yang Zhao, Ting Zhao, Jingyang Guan, Xu Zhang, Yao Fu, Junqing Ye, Jialiang Zhu, Gaofan Meng, Jian Ge, Susu Yang, Lin Cheng, Yaqin Du, Chaoran Zhao, Ting Wang, Linlin Su, Weifeng Yang, Hongkui Deng

DOI: http://dx.doi.org/10.1016/j.cell.2015.11.017

Cell, Vol. 163, Issue 7, p1678–1691

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xIn the process of chemical reprogramming from somatic cells to pluripotent stem cells, an intermediate extraembryonic endoderm (XEN)-like state is uncovered, allowing the development of a robust chemical reprogramming system by manipulating small molecules more precisely through this unique route.

封面文章：siRNA生成对拟南芥DNA甲基化的调控

A Dicer-Independent Route for Biogenesis of siRNAs that Direct DNA Methylation in Arabidopsis

Article

Ruiqiang Ye, Zulong Chen, Bi Lian, M. Jordan Rowley, Ning Xia, Jijie Chai, Yan Li, Xin-Jian He, Andrzej T. Wierzbicki, Yijun Qi

DOI: http://dx.doi.org/10.1016/j.molcel.2015.11.015

Molecular Cell, Vol. 61, Issue 2, p222–235

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xIn plants, DNA methylation can be directed by 24-nt siRNAs that are produced by DCL3. Ye et al. report a distinct class of DCL-independent siRNAs, sidRNAs. sidRNAs interact with AGO4 and require distributive 3′-5′ exonucleases for their biogenesis. The authors propose that sidRNAs are the initial triggers of de novo DNA methylation.

Abiotic Stress Signaling and Responses in Plants
Review
Jian-Kang Zhu
DOI: http://dx.doi.org/10.1016/j.cell.2016.08.029
Cell, Vol. 167, Issue 2, p313–324
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xUnderstanding the core set of pathways that allow plants to cope with abiotic stresses such as salinity, drought, and extreme temperatures can allow us to improve crop sustainability and food security for a growing world population.

Feedback Activation of Leukemia Inhibitory Factor Receptor Limits Response to Histone Deacetylase Inhibitors in Breast Cancer
Article
Hanlin Zeng, Jia Qu, Nan Jin, Jun Xu, Chenchu Lin, Yi Chen, Xinying Yang, Xiang He, Shuai Tang, Xiaojing Lan, Xiaotong Yang, Ziqi Chen, Min Huang, Jian Ding, Meiyu Geng
DOI: http://dx.doi.org/10.1016/j.ccell.2016.08.001
Cancer Cell, Vol. 30, Issue 3, p459–473
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xZeng et al. show that HDAC inhibitors (HDACi) promote BRD4-mediated activation of LIFR, which in turn activates JAK1-STAT3 signaling and restrains the efficacy of HDACi in breast cancer. Concurrent inhibition of BRD4 or JAK sensitizes breast cancer, in particular the triple-negative subset, to HDACi.

Tumor Exosomal RNAs Promote Lung Pre-metastatic Niche Formation by Activating Alveolar Epithelial TLR3 to Recruit Neutrophils
Article
Yanfang Liu, Yan Gu, Yanmei Han, Qian Zhang, Zhengping Jiang, Xiang Zhang, Bo Huang, Xiaoqing Xu, Jianming Zheng, Xuetao Cao
DOI: http://dx.doi.org/10.1016/j.ccell.2016.06.021
Cancer Cell, Vol. 30, Issue 2, p243–256
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xLiu et al. demonstrate that TLR3 in host alveolar epithelial cells is critical for neutrophil recruitment and lung pre-metastatic niche formation. Mechanistically, small nuclear RNAs from primary tumor-derived exosomes activate TLR3, which leads to chemokine secretion and neutrophil infiltration.