Tuesday, July 3, 2018

Nature Cell Biology contents: July 2018 Volume 20 Number 7

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TABLE OF CONTENTS

July 2018 Volume 20, Issue 7

Editorial
News & Views
Review Articles
Letters
Articles
Resources
 
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Editorial

 

Focusing on mitochondrial form and function    p735
doi:10.1038/s41556-018-0139-7

News & Views

 

Pro-tumorigenic AMPK in glioblastoma    pp736 - 737
Nektaria Maria Leli & Constantinos Koumenis
doi:10.1038/s41556-018-0129-9

Grasping for aspartate in tumour metabolism    pp738 - 739
Accalia Fu & Nika N. Danial
doi:10.1038/s41556-018-0137-9

GNAS shifts metabolism in pancreatic cancer    pp740 - 741
Pablo E. Hollstein & Reuben J. Shaw
doi:10.1038/s41556-018-0120-5

A single-cell chromatin map of human embryos    pp742 - 744
Raquel Pérez-Palacios & Deborah Bourc'his
doi:10.1038/s41556-018-0134-z

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Review Articles

 

The multifaceted contributions of mitochondria to cellular metabolism    pp745 - 754
Jessica B. Spinelli & Marcia C. Haigis
doi:10.1038/s41556-018-0124-1

Mitochondrial dynamics in adaptive and maladaptive cellular stress responses    pp755 - 765
Verónica Eisner, Martin Picard & György Hajnóczky
doi:10.1038/s41556-018-0133-0

Mitochondria sense and respond to many stressors and can support cell survival or death through energy production and signalling pathways. Mitochondrial responses depend on fusion–fission dynamics that dilute and segregate damaged mitochondria. Mitochondrial motility and inter-organellar interactions, such as with the endoplasmic reticulum, also function in cellular adaptation to stress. In this Review, we discuss how stressors influence these components, and how they contribute to the complex adaptive and pathological responses that lead to disease.

 

Mechanisms and impact of altered tumour mechanics    pp766 - 774
Hamid Mohammadi & Erik Sahai
doi:10.1038/s41556-018-0131-2

Tumours are often more stiff than normal tissue. In this Review, Mohammadi and Sahai discuss recent insights into how such altered tumour mechanics arise and how this affects tumorigenesis.

 

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Letters

 

Aspartate is a limiting metabolite for cancer cell proliferation under hypoxia and in tumours    pp775 - 781
Javier Garcia-Bermudez, Lou Baudrier, Konnor La, Xiphias Ge Zhu, Justine Fidelin et al.
doi:10.1038/s41556-018-0118-z

Garcia-Bermudez et al. and Sullivan et al. show that endogenous aspartate is a limiting metabolite for cancer cell proliferation under hypoxia and in tumours, and that metformin depletes aspartate to limit tumour growth.

 

Aspartate is an endogenous metabolic limitation for tumour growth    pp782 - 788
Lucas B. Sullivan, Alba Luengo, Laura V. Danai, Lauren N. Bush, Frances F. Diehl et al.
doi:10.1038/s41556-018-0125-0

Garcia-Bermudez et al. and Sullivan et al. show that endogenous aspartate is a limiting metabolite for cancer cell proliferation under hypoxia and in tumours, and that metformin depletes aspartate to limit tumour growth.

 

Articles

 

Senescence-associated ribosome biogenesis defects contributes to cell cycle arrest through the Rb pathway    pp789 - 799
Frédéric Lessard, Sebastian Igelmann, Christian Trahan, Geneviève Huot, Emmanuelle Saint-Germain et al.
doi:10.1038/s41556-018-0127-y

Lassard et al. demonstrate a relationship between cellular senescence and perturbed ribosome biogenesis and find that the ribosomal protein S14 is an inhibitor of CDK4, inducing an Rb-dependent cell cycle arrest.

 

Dynamic kinetochore size regulation promotes microtubule capture and chromosome biorientation in mitosis    pp800 - 810
Carlos Sacristan, Misbha Ud Din Ahmad, Jenny Keller, Job Fermie, Vincent Groenewold et al.
doi:10.1038/s41556-018-0130-3

Sacristan et al. show that the dynein adaptor Spindly facilitates oligomerisation of the RZZ complex to expand the kinetochore, after which Spindly-associated dynein compacts the kinetochore to allow for faithful chromosome segregation.

 

Mutant GNAS drives pancreatic tumourigenesis by inducing PKA-mediated SIK suppression and reprogramming lipid metabolism    pp811 - 822
Krushna C. Patra, Yasutaka Kato, Yusuke Mizukami, Sebastian Widholz, Myriam Boukhali et al.
doi:10.1038/s41556-018-0122-3

Bardeesy and colleagues show that mutant GNAS suppresses salt-inducible kinases by activating PKA, leading to lipid remodelling and pancreatic tumourigenesis

 

AMP kinase promotes glioblastoma bioenergetics and tumour growth    pp823 - 835
Rishi Raj Chhipa, Qiang Fan, Jane Anderson, Ranjithmenon Muraleedharan, Yan Huang et al.
doi:10.1038/s41556-018-0126-z

Signalling by the energy sensor kinase AMPK is generally tumour suppressive, but Chhipa et al. show that AMPK is upregulated in glioblastoma, where it phosphorylates CREB1 to enhance HIF1a and GABPA transcription and to support tumour bioenergetics.

 

Resources

 

Single-cell characterization of haematopoietic progenitors and their trajectories in homeostasis and perturbed haematopoiesis    pp836 - 846
Amir Giladi, Franziska Paul, Yoni Herzog, Yaniv Lubling, Assaf Weiner et al.
doi:10.1038/s41556-018-0121-4

Using a multi-tier scRNA-seq and CRISP-seq approach, Giladi et al. define a transcriptional signature for the naive haematopoietic stem cell state, and follow progenitor plasticity and fate commitment under the influence of cytokines and growth factors.

 

Single-cell multi-omics sequencing of human early embryos    pp847 - 858
Lin Li, Fan Guo, Yun Gao, Yixin Ren, Peng Yuan et al.
doi:10.1038/s41556-018-0123-2

Using scCOOL-seq, Li et al. simultaneously characterize the DNA methylation and chromatin accessibility of the same cell during human preimplantation development.

 

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Nature Research Custom Media presents a webcast on: Practical Considerations for T Cell Receptor (TCR) Therapies Targeting Solid Tumors

Date: Tuesday, July 17, 2018

Join the webcast to learn about the advantages of automated cell cloning and methods for rapid cloning and validation of functional TCRs.

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