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2015/01/30

Nature Cell Biology contents: February 2015 Volume 17 Number 2, pp 107 - 194

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Nature Cell Biology

TABLE OF CONTENTS

February 2015 Volume 17, Issue 2

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A niche role for periostin and macrophages in glioblastoma   pp107 - 109
Mario Leonardo Squadrito and Michele De Palma
doi:10.1038/ncb3095
Macrophages facilitate tumour progression, but it is unclear whether this capability is influenced by tumour-initiating cells. Glioblastoma stem cells are now shown to secrete periostin, a matrix protein that recruits protumoral macrophages and enhances glioblastoma progression in mice.

See also: Article by Zhou et al.

Control of ciliation in embryogenesis   pp109 - 111
Anna S. Nikonova and Erica A. Golemis
doi:10.1038/ncb3103
The protrusion of cilia into extracellular space provides cells with sensors of localized environmental cues that include fluid flow, mechanical force and important growth factors such as Hedgehog. Live imaging has now captured the initial appearance of cilia during embryogenesis, and defined lineage-specific determinants that restrict extra-embryonal ciliogenesis.

See also: Article by Bangs et al.

Articles

Lineage specificity of primary cilia in the mouse embryo   pp113 - 122
Fiona K. Bangs, Nadine Schrode, Anna-Katerina Hadjantonakis and Kathryn V. Anderson
doi:10.1038/ncb3091
Anderson and colleagues report that, although mouse embryonic tissues form primary cilia, in cells destined for extraembryonic lineages, the activities of aurora kinase A and the tubulin deacetylase HDAC6 inhibit ciliogenesis.

See also: News and Views by Nikonova & Golemis

Platelet-derived SDF-1 primes the pulmonary capillary vascular niche to drive lung alveolar regeneration   pp123 - 136
Shahin Rafii, Zhongwei Cao, Raphael Lis, Ilias I. Siempos, Deebly Chavez et al.
doi:10.1038/ncb3096
Ding and colleagues report that blood platelets recruited to the lung by injury release the chemokine SDF-1, which interacts with its receptor CXCR4 on pulmonary capillary endothelial cells and thereby initiates alveolar regeneration.

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Myosin II controls cellular branching morphogenesis and migration in three dimensions by minimizing cell-surface curvature   pp137 - 147
Hunter Elliott, Robert S. Fischer, Kenneth A. Myers, Ravi A. Desai, Lin Gao et al.
doi:10.1038/ncb3092
Elliott et al. use high-resolution imaging, microfabrication and computational analyses to show that the interplay between cell-surface curvature and activity and cortical recruitment of myosin II, control cell migration in 3D matrices.

Cdk1-dependent mitotic enrichment of cortical myosin II promotes cell rounding against confinement   pp148 - 159
Subramanian P. Ramanathan, Jonne Helenius, Martin P. Stewart, Cedric J. Cattin, Anthony A. Hyman et al.
doi:10.1038/ncb3098
Hyman, Muller and colleagues characterize how mitotic rounding forces relate to the dynamics of the actomyosin cortex. They find that myosin II enables the cell to resist deformation.

USP30 and parkin homeostatically regulate atypical ubiquitin chains on mitochondria   pp160 - 169
Christian N. Cunningham, Joshua M. Baughman, Lilian Phu, Joy S. Tea, Christine Yu et al.
doi:10.1038/ncb3097
Cunningham et al. characterize the ubiquitin chain linkages regulated by the opposing activities of the E3 ligase parkin and the deubiquitylation enzyme USP30 on mitochondria.

Periostin secreted by glioblastoma stem cells recruits M2 tumour-associated macrophages and promotes malignant growth   pp170 - 182
Wenchao Zhou, Susan Q. Ke, Zhi Huang, William Flavahan, Xiaoguang Fang et al.
doi:10.1038/ncb3090
Bao and colleagues report that glioblastoma cancer stem cells produce periostin, which in turn recruits tumour-associated macrophages to the tumour site to foster growth.

See also: News and Views by Squadrito & De Palma

Breast-cancer-secreted miR-122 reprograms glucose metabolism in premetastatic niche to promote metastasis   pp183 - 194
Miranda Y. Fong, Weiying Zhou, Liang Liu, Aileen Y. Alontaga, Manasa Chandra et al.
doi:10.1038/ncb3094
Wang and colleagues report that cancer-cell-derived extracellular vesicles that contain miR-122 reprogram glucose metabolism of premetastatic niche cells to alter nutrient availability and promote metastasis.

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