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2016/07/27

Nature Cell Biology contents: August 2016 Volume 18 Number 8, pp 823 - 909

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TABLE OF CONTENTS

August 2016 Volume 18, Issue 8

Review
News and Views
Articles
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Review

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Metabolic regulation of stem cell function in tissue homeostasis and organismal ageing   pp823 - 832
Navdeep S. Chandel, Heinrich Jasper, Theodore T. Ho and Emmanuelle Passegue
doi:10.1038/ncb3385
Passegue and colleagues discuss recent advances in our understanding of the metabolic control of stem cell function, and how stem cell metabolism relates to homeostasis and ageing.

News and Views

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p53 mutations promote proteasomal activity   pp833 - 835
Moshe Oren and Eran Kotler
doi:10.1038/ncb3392
p53 mutations occur very frequently in human cancer. Besides abrogating the tumour suppressive functions of wild-type p53, many of those mutations also acquire oncogenic gain-of-function activities. Augmentation of proteasome activity is now reported as a common gain-of-function mechanism shared by different p53 mutants, which promotes cancer resistance to proteasome inhibitors.

See also: Article by Walerych et al.

Hippo's Q for a big liver   pp835 - 837
Dimitrios Anastasiou
doi:10.1038/ncb3391
The Hippo pathway is a key regulator of organ size that has also been implicated in tumorigenesis. Yap, one of the effectors of Hippo signalling, is now reported to support these functions by promoting glutamine synthesis.

See also: Article by Cox et al.

Articles

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Autophagosome-lysosome fusion triggers a lysosomal response mediated by TLR9 and controlled by OCRL   pp839 - 850
Maria Giovanna De Leo, Leopoldo Staiano, Mariella Vicinanza, Alessandro Luciani, Annamaria Carissimo et al.
doi:10.1038/ncb3386
De Leo et al. identify a lysosomal response to autophagic cargo during lysosome-autophagosome fusion that involves TLR9 activation and OCRL recruitment, and leads to a regulated local increase in PtdIns(4,5)P2, which is necessary for a normal autophagic flux.

Cathepsin-B-mediated cleavage of Disabled-2 regulates TGF-β-induced autophagy   pp851 - 863
Yong Jiang, Alec N. Woosley, Nageswaran Sivalingam, Sneha Natarajan and Philip H. Howe
doi:10.1038/ncb3388
Jiang et al. show that Disabled-2 (Dab2) regulates the switch between autophagy and apoptosis in TGB-β-treated cells, through regulation of the Beclin-1-Vps34 interaction.

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Mechanical regulation of transcription controls Polycomb-mediated gene silencing during lineage commitment   pp864 - 875
Huy Quang Le, Sushmita Ghatak, Ching-Yan Chloe Yeung, Frederik Tellkamp, Christian Gunschmann et al.
doi:10.1038/ncb3387
Wickstrom and colleagues describe how mechanical forces applied to epidermal stem cells lead to relocation of emerin to the nuclear envelope and reduced nuclear actin levels, resulting in chromatin changes that influence lineage commitment.

F-actin dismantling through a redox-driven synergy between Mical and cofilin   pp876 - 885
Elena E. Grintsevich, Hunkar Gizem Yesilyurt, Shannon K. Rich, Ruei-Jiun Hung, Jonathan R. Terman et al.
doi:10.1038/ncb3390
Grintsevich et al. discover that the redox enzyme Mical oxidizes F-actin to promote binding of the F-actin-severing protein cofilin, and that the synergy of Mical and cofilin is necessary and sufficient for F-actin disassembly in Drosophila.

Yap reprograms glutamine metabolism to increase nucleotide biosynthesis and enable liver growth   pp886 - 896
Andrew G. Cox, Katie L. Hwang, Kristin K. Brown, Kimberley J. Evason, Sebastian Beltz et al.
doi:10.1038/ncb3389
Cox et al. report that Yap induces the expression of glutamine synthetase, thereby elevating glutamine and nitrogen levels for de novo nucleotide synthesis. They show that this promotes hepatomegaly and growth of liver cancer cells in zebrafish.

See also: News and Views by Anastasiou

Proteasome machinery is instrumental in a common gain-of-function program of the p53 missense mutants in cancer   pp897 - 909
Dawid Walerych, Kamil Lisek, Roberta Sommaggio, Silvano Piazza, Yari Ciani et al.
doi:10.1038/ncb3380
Walerych et al. show that p53 missense mutants upregulate the proteasome and increase breast cancer cell resistance to proteasome inhibitors. Combined inhibition of p53 mutants and the proteasome leads to increased therapeutic efficacy.

See also: News and Views by Oren & Kotler

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