Nature Cell Biology contents: May 2016 Volume 18 Number 5, pp 459 - 578

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Advertisement nature.com webcasts Nature Publishing Group presents a custom webcast on Advances in neuroscience: New methods for correlating structure and function Thursday May 5, 2016 8AM PDT, 10AM CDT, 11AM EDT, 4PM BST, 5PM CEST  Register for the webcast and live Q&A session Sponsored by: Leica Microsystems   TABLE OF CONTENTS May 2016 Volume 18, Issue 5 News and Views Articles Letter Advertisement  Are you sure your cells are really alive? Find your zombie cells using Apoptag® apoptosis detection assays. If your assay only detects the late stage of apoptosis, you may be a victim of the zombie cell apocalypse. Apoptosis occurs in a variety of stages. Over 10,000 publications have used Apoptag® assays to detect cell death events with better sensitivity and reproducibility than exclusion dyes like.  Zombie Apocalypse Survival Tool Kit Subscribe   Facebook   RSS   Recommend to library   Twitter   Advertisement Established as a sister journal of Cell Research, Cell Discovery is a fully open access journal publishing original articles and reviews on results of significance and originality in all areas of molecular and cell biology.  Submit your manuscript   News and Views Top The molecular clutch model for mechanotransduction evolves   pp459 - 461 Vinay Swaminathan and Clare M. Waterman doi:10.1038/ncb3350 Many biological processes are influenced by the mechanical rigidity of surrounding tissues. Now, a combination of experiments and mathematical modelling has been used to describe the precise molecular and physical mechanism by which cells sense and respond to the mechanical properties of their extracellular environment through integrin-based adhesions. See also: Article by Elosegui-Artola et al. Directing lipid transport at membrane contact sites   pp461 - 463 Michael Krauβ and Volker Haucke doi:10.1038/ncb3345 Contact sites between the endoplasmic reticulum and the plasma membrane mediate receptor signalling. How this function is controlled physically and functionally is poorly understood. Extended synaptotagmins are now shown to shuttle the lipid metabolite diacylglycerol from the plasma membrane to the endoplasmic reticulum in receptor-stimulated cells. See also: Article by Saheki et al. Orchestrating Wnt signalling for metabolic liver zonation   pp463 - 465 Walter Birchmeier doi:10.1038/ncb3349 Wnt/β-catenin signalling is an important regulator of liver development, zonation and regeneration. The cell surface complex RSPO-LGR4/5-ZNF3/RNF43 is now shown to direct Wnt/β-catenin signalling in orchestrating the division of the liver into functionally distinct metabolic zones, providing insights into the mechanisms that influence organ development and regeneration. See also: Article by Planas-Paz et al. Fibroblasts form a hospitable metastatic niche in the liver   pp465 - 466 Neta Erez doi:10.1038/ncb3352 The liver is the most common metastatic route of pancreatic cancer. Early recruitment of granulin-secreting inflammatory monocytes to the liver is now shown to reprogram hepatic stellate cells into myofibroblasts that modulate the liver microenvironment to support the growth of metastasizing tumour cells. See also: Article by Nielsen et al. Cell Biology JOBS of the week Faculty Positions in Neuroscience and Cell Biology The University of Texas Medical Branch (UTMB Health) Single-Cell Molecular / Microfluidics Biology Post-Docs California Institute of Technology Postdoctoral Position Stem Cell Biology and Tissue Engineering Northwestern University More Science jobs from Cell Biology EVENT Physical Biology of the Cell 18.09.16 Woods Hole, USA More science events from Articles Top The RSPO–LGR4/5–ZNRF3/RNF43 module controls liver zonation and size   pp467 - 479 Lara Planas-Paz, Vanessa Orsini, Luke Boulter, Diego Calabrese, Monika Pikiolek et al. doi:10.1038/ncb3337 Tchorz and colleagues identify a role for the RSPO–LGR4/5–ZNRF3/RNF43 module as master regulator of Wnt/β-catenin-mediated metabolic liver zonation and hepatic growth/size control during development, homeostasis and regeneration. See also: News and Views by Birchmeier Per2 induction limits lymphoid-biased haematopoietic stem cells and lymphopoiesis in the context of DNA damage and ageing   pp480 - 490 Jianwei Wang, Yohei Morita, Bing Han, Silke Niemann, Bettina Loffler et al. doi:10.1038/ncb3342 Rudolph and colleagues identify Per2 as a negative regulator of lymphoid-biased haematopoietic stem cells, and show that it reduces cell maintenance and function in response to DNA damage and ageing. FAK, talin and PIPKIγ regulate endocytosed integrin activation to polarize focal adhesion assembly   pp491 - 503 Guilherme P. F. Nader, Ellen J. Ezratty and Gregg G. Gundersen doi:10.1038/ncb3333 Gundersen and colleagues report that FAK, talin and PIPKIγ maintain the active conformation of integrin that is internalized in Rab11 recycling endosomes, to polarize focal adhesion assembly for directed cell migration. Control of plasma membrane lipid homeostasis by the extended synaptotagmins   pp504 - 515 Yasunori Saheki, Xin Bian, Curtis M. Schauder, Yujin Sawaki, Michal A. Surma et al. doi:10.1038/ncb3339 Saheki and colleagues show that extended synaptotagmins (E-Syts), ER proteins that function as tethers to the plasma membrane, can transfer lipids between bilayers in a Ca2+- and SMP-domain-dependent manner, thus regulating plasma membrane lipid homeostasis. See also: News and Views by Krauβ & Haucke The Aurora-B-dependent NoCut checkpoint prevents damage of anaphase bridges after DNA replication stress   pp516 - 526 Nuno Amaral, Alexandre Vendrell, Charlotta Funaya, Fatima-Zahra Idrissi, Michael Maier et al. doi:10.1038/ncb3343 Mendoza and colleagues provide insights into the specificity of the NoCut checkpoint, showing that although different types of chromosomal defects delay cytokinetic abscission, only after replication stress does this prevent DNA damage. HSF1 critically attunes proteotoxic stress sensing by mTORC1 to combat stress and promote growth   pp527 - 539 Kuo-Hui Su, Junyue Cao, Zijian Tang, Siyuan Dai, Yishu He et al. doi:10.1038/ncb3335 Dai and colleagues reveal that proteotoxic stress causes JNK-mediated disintegration of the mTORC1 complexes, whereas heat shock factor 1 (HSF1) counteracts this response to promote stress resistance and growth. Mechanical regulation of a molecular clutch defines force transmission and transduction in response to matrix rigidity   pp540 - 548 Alberto Elosegui-Artola, Roger Oria, Yunfeng Chen, Anita Kosmalska, Carlos Pérez-González et al. doi:10.1038/ncb3336 Integrins and talin are parts of a 'molecular clutch' that mechanically links the actin cytoskeleton to the extracellular matrix. Elosegui-Artola et al. now reveal a tunable rigidity threshold, above which talin unfolds to mediate force transduction. See also: News and Views by Swaminathan & Waterman Macrophage-secreted granulin supports pancreatic cancer metastasis by inducing liver fibrosis   pp549 - 560 Sebastian R. Nielsen, Valeria Quaranta, Andrea Linford, Perpetua Emeagi, Carolyn Rainer et al. doi:10.1038/ncb3340 Nielsen et al. show that granulin is secreted by metastasis-associated macrophages to promote pancreatic cancer metastasis. Granulin activates hepatic stellate cells, which secrete periostin, thereby resulting in a fibrotic, pro-metastatic liver milieu. See also: News and Views by Erez A splicing switch from ketohexokinase-C to ketohexokinase-A drives hepatocellular carcinoma formation   pp561 - 571 Xinjian Li, Xu Qian, Li-Xia Peng, Yuhui Jiang, David H. Hawke et al. doi:10.1038/ncb3338 Li et al. show that the c-Myc-dependent splicing switch from ketohexokinase-C (KHK-C) to KHK-A activates phosphoribosyl pyrophosphate synthetase 1 (PRPS1), resulting in enhanced de novo nucleic acid synthesis and hepatocellular carcinoma formation. Letter Top Glutathione biosynthesis is a metabolic vulnerability in PI(3)K/Akt-driven breast cancer   pp572 - 578 Evan C. Lien, Costas A. Lyssiotis, Ashish Juvekar, Hai Hu, John M. Asara et al. doi:10.1038/ncb3341 Lien et al. show that oncogenic PI(3)K/Akt signalling stimulates glutathione (GSH) synthesis by activation of the transcription factor Nrf2 and regulation of GSH biosynthesis genes in breast cancer. 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