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Nature Cell Biology

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https://www.readbyqxmd.com/read/29131140/a-transient-pool-of-nuclear-f-actin-at-mitotic-exit-controls-chromatin-organization
#1
Christian Baarlink, Matthias Plessner, Alice Sherrard, Kohtaro Morita, Shinji Misu, David Virant, Eva-Maria Kleinschnitz, Robert Harniman, Dominic Alibhai, Stefan Baumeister, Kei Miyamoto, Ulrike Endesfelder, Abderrahmane Kaidi, Robert Grosse
Re-establishment of nuclear structure and chromatin organization after cell division is integral for genome regulation or development and is frequently altered during cancer progression. The mechanisms underlying chromatin expansion in daughter cells remain largely unclear. Here, we describe the transient formation of nuclear actin filaments (F-actin) during mitotic exit. These nuclear F-actin structures assemble in daughter cell nuclei and undergo dynamic reorganization to promote nuclear protrusions and volume expansion throughout early G1 of the cell cycle...
November 13, 2017: Nature Cell Biology
https://www.readbyqxmd.com/read/29084199/class-iii-phosphatidylinositol-3-oh-kinase-controls-epithelial-integrity-through-endosomal-lkb1-regulation
#2
Fergal O'Farrell, Viola Hélène Lobert, Marte Sneeggen, Ashish Jain, Nadja Sandra Katheder, Eva Maria Wenzel, Sebastian Wolfgang Schultz, Kia Wee Tan, Andreas Brech, Harald Stenmark, Tor Erik Rusten
The molecular mechanisms underlying the interdependence between intracellular trafficking and epithelial cell polarity are poorly understood. Here we show that inactivation of class III phosphatidylinositol-3-OH kinase (CIII-PI3K), which produces phosphatidylinositol-3-phosphate (PtdIns3P) on endosomes, disrupts epithelial organization. This is caused by dysregulation of endosomally localized Liver Kinase B1 (LKB1, also known as STK11), which shows delocalized and increased activity accompanied by dysplasia-like growth and invasive behaviour of cells provoked by JNK pathway activation...
October 30, 2017: Nature Cell Biology
https://www.readbyqxmd.com/read/29084198/distinct-kinetics-of-serine-and-threonine-dephosphorylation-are-essential-for-mitosis
#3
Jamin B Hein, Emil P T Hertz, Dimitriya H Garvanska, Thomas Kruse, Jakob Nilsson
Protein phosphatase 2A (PP2A) in complex with B55 regulatory subunits reverses cyclin-dependent kinase 1 (Cdk1) phosphorylations at mitotic exit. Interestingly, threonine and serine residues phosphorylated by Cdk1 display distinct phosphorylation dynamics, but the biological significance remains unexplored. Here we demonstrate that the phosphothreonine preference of PP2A-B55 provides an essential regulatory element of mitotic exit. To allow rapid activation of the anaphase-promoting complex/cyclosome (APC/C) co-activator Cdc20, inhibitory phosphorylation sites are conserved as threonines while serine substitutions delay dephosphorylation and Cdc20 activation...
October 30, 2017: Nature Cell Biology
https://www.readbyqxmd.com/read/29084197/tbc1d23-is-a-bridging-factor-for-endosomal-vesicle-capture-by-golgins-at-the-trans-golgi
#4
John J H Shin, Alison K Gillingham, Farida Begum, Jessica Chadwick, Sean Munro
The specificity of membrane traffic involves tethers at destination organelles that selectively capture incoming transport vesicles to allow SNAREs on opposing membranes to then assemble and drive fusion. Tethers include both protein complexes and long coiled-coil proteins, although how they contribute to specificity remains unclear. The golgin coiled-coil proteins at the Golgi apparatus capture vesicles from different origins, but the vesicle-specific molecular cues that they recognize are unknown. Vesicle tethering is typically a transient process and therefore is challenging to interrogate in vivo...
October 30, 2017: Nature Cell Biology
https://www.readbyqxmd.com/read/29058721/egfr-signalling-controls-cellular-fate-and-pancreatic-organogenesis-by-regulating-apicobasal-polarity
#5
Zarah M Löf-Öhlin, Pia Nyeng, Matthew E Bechard, Katja Hess, Eric Bankaitis, Thomas U Greiner, Jacqueline Ameri, Christopher V Wright, Henrik Semb
Apicobasal polarity is known to affect epithelial morphogenesis and cell differentiation, but it remains unknown how these processes are mechanistically orchestrated. We find that ligand-specific EGFR signalling via PI(3)K and Rac1 autonomously modulates apicobasal polarity to enforce the sequential control of morphogenesis and cell differentiation. Initially, EGF controls pancreatic tubulogenesis by negatively regulating apical polarity induction. Subsequently, betacellulin, working via inhibition of atypical protein kinase C (aPKC), causes apical domain constriction within neurogenin3(+) endocrine progenitors, which results in reduced Notch signalling, increased neurogenin3 expression, and β-cell differentiation...
November 2017: Nature Cell Biology
https://www.readbyqxmd.com/read/29058720/the-impact-of-cellular-metabolism-on-chromatin-dynamics-and-epigenetics
#6
REVIEW
Michael A Reid, Ziwei Dai, Jason W Locasale
The substrates used to modify nucleic acids and chromatin are affected by nutrient availability and the activity of metabolic pathways. Thus, cellular metabolism constitutes a fundamental component of chromatin status and thereby of genome regulation. Here we describe the biochemical and genetic principles of how metabolism can influence chromatin biology and epigenetics, discuss the functional roles of this interplay in developmental and cancer biology, and present future directions in this rapidly emerging area...
November 2017: Nature Cell Biology
https://www.readbyqxmd.com/read/29058719/synthetic-hydrogels-for-human-intestinal-organoid-generation-and-colonic-wound-repair
#7
Ricardo Cruz-Acuña, Miguel Quirós, Attila E Farkas, Priya H Dedhia, Sha Huang, Dorothée Siuda, Vicky García-Hernández, Alyssa J Miller, Jason R Spence, Asma Nusrat, Andrés J García
In vitro differentiation of human intestinal organoids (HIOs) from pluripotent stem cells is an unparalleled system for creating complex, multicellular three-dimensional structures capable of giving rise to tissue analogous to native human tissue. Current methods for generating HIOs rely on growth in an undefined tumour-derived extracellular matrix (ECM), which severely limits the use of organoid technologies for regenerative and translational medicine. Here, we developed a fully defined, synthetic hydrogel based on a four-armed, maleimide-terminated poly(ethylene glycol) macromer that supports robust and highly reproducible in vitro growth and expansion of HIOs, such that three-dimensional structures are never embedded in tumour-derived ECM...
November 2017: Nature Cell Biology
https://www.readbyqxmd.com/read/29058718/pkm2-methylation-by-carm1-activates-aerobic-glycolysis-to-promote-tumorigenesis
#8
Fabao Liu, Fengfei Ma, Yuyuan Wang, Ling Hao, Hao Zeng, Chenxi Jia, Yidan Wang, Peng Liu, Irene M Ong, Baobin Li, Guojun Chen, Jiaoyang Jiang, Shaoqin Gong, Lingjun Li, Wei Xu
Metabolic reprogramming is a hallmark of cancer. Herein we discover that the key glycolytic enzyme pyruvate kinase M2 isoform (PKM2), but not the related isoform PKM1, is methylated by co-activator-associated arginine methyltransferase 1 (CARM1). PKM2 methylation reversibly shifts the balance of metabolism from oxidative phosphorylation to aerobic glycolysis in breast cancer cells. Oxidative phosphorylation depends on mitochondrial calcium concentration, which becomes critical for cancer cell survival when PKM2 methylation is blocked...
November 2017: Nature Cell Biology
https://www.readbyqxmd.com/read/29035360/ezh2-promotes-degradation-of-stalled-replication-forks-by-recruiting-mus81-through-histone-h3-trimethylation
#9
Beatrice Rondinelli, Ewa Gogola, Hatice Yücel, Alexandra A Duarte, Marieke van de Ven, Roxanne van der Sluijs, Panagiotis A Konstantinopoulos, Jos Jonkers, Raphaël Ceccaldi, Sven Rottenberg, Alan D D'Andrea
The emergence of resistance to poly-ADP-ribose polymerase inhibitors (PARPi) poses a threat to the treatment of BRCA1 and BRCA2 (BRCA1/2)-deficient tumours. Stabilization of stalled DNA replication forks is a recently identified PARPi-resistance mechanism that promotes genomic stability in BRCA1/2-deficient cancers. Dissecting the molecular pathways controlling genomic stability at stalled forks is critical. Here we show that EZH2 localizes at stalled forks where it methylates Lys27 on histone 3 (H3K27me3), mediating recruitment of the MUS81 nuclease...
November 2017: Nature Cell Biology
https://www.readbyqxmd.com/read/29035359/acute-myeloid-leukaemia-disrupts-endogenous-myelo-erythropoiesis-by-compromising-the-adipocyte-bone-marrow-niche
#10
Allison L Boyd, Jennifer C Reid, Kyle R Salci, Lili Aslostovar, Yannick D Benoit, Zoya Shapovalova, Mio Nakanishi, Deanna P Porras, Mohammed Almakadi, Clinton J V Campbell, Michael F Jackson, Catherine A Ross, Ronan Foley, Brian Leber, David S Allan, Mitchell Sabloff, Anargyros Xenocostas, Tony J Collins, Mickie Bhatia
Acute myeloid leukaemia (AML) is distinguished by the generation of dysfunctional leukaemic blasts, and patients characteristically suffer from fatal infections and anaemia due to insufficient normal myelo-erythropoiesis. Direct physical crowding of bone marrow (BM) by accumulating leukaemic cells does not fully account for this haematopoietic failure. Here, analyses from AML patients were applied to both in vitro co-culture platforms and in vivo xenograft modelling, revealing that human AML disease specifically disrupts the adipocytic niche in BM...
November 2017: Nature Cell Biology
https://www.readbyqxmd.com/read/28991221/a-non-coding-function-of-tyrp1-mrna-promotes-melanoma-growth
#11
David Gilot, Mélodie Migault, Laura Bachelot, Fabrice Journé, Aljosja Rogiers, Emmanuelle Donnou-Fournet, Ariane Mogha, Nicolas Mouchet, Marie-Laure Pinel-Marie, Bernard Mari, Tristan Montier, Sébastien Corre, Arthur Gautron, Florian Rambow, Petra El Hajj, Rania Ben Jouira, Sophie Tartare-Deckert, Jean-Christophe Marine, Brice Felden, Ghanem Ghanem, Marie-Dominique Galibert
Competition among RNAs to bind miRNA is proposed to influence biological systems. However, the role of this competition in disease onset is unclear. Here, we report that TYRP1 mRNA, in addition to encoding tyrosinase-related protein 1 (TYRP1), indirectly promotes cell proliferation by sequestering miR-16 on non-canonical miRNA response elements. Consequently, the sequestered miR-16 is no longer able to repress its mRNA targets, such as RAB17, which is involved in melanoma cell proliferation and tumour growth...
November 2017: Nature Cell Biology
https://www.readbyqxmd.com/read/29087386/tyrp1-mrna-goes-fishing-for-mirnas-in-melanoma
#12
Maria S Soengas, Eva Hernando
A variety of non-coding RNAs have been reported as endogenous sponges for cancer-modulating miRNAs. However, miRNA trapping by transcripts with protein-coding functions is less understood. The mRNA of TYRP1 is now found to sequester the tumour suppressor miR-16 on non-canonical miRNA response elements in melanoma, thereby promoting malignant growth.
October 31, 2017: Nature Cell Biology
https://www.readbyqxmd.com/read/29087385/implantable-synthetic-organoid-matrices-for-intestinal-regeneration
#13
Jeffrey W Brown, Jason C Mills
Organoids are a powerful tool to study both physiological and disease processes. A completely synthetic matrix assembled from exchangeable modular parts has been developed and not only supports proliferation of human intestinal organoids derived from pluripotent embryonic stem cells, but also augments subsequent ad vivo implantation into injured murine colon.
October 31, 2017: Nature Cell Biology
https://www.readbyqxmd.com/read/29087384/parpi-focus-the-spotlight-on-replication-fork-protection-in-cancer
#14
Katharina Schlacher
PARP inhibitors (PARPi) kill BRCA1/2-mutated cancers, which become resistant when DNA repair functions are restored. Now, MUS81 nuclease inhibition due to EZH2 downregulation is found to restore DNA replication fork protection but not repair, leading to PARPi-resistance in mutant BRCA2 cells and patients. This challenges the DNA repair dominance in synthetic lethality.
October 31, 2017: Nature Cell Biology
https://www.readbyqxmd.com/read/29087383/erratum-super-resolution-microscopy-reveals-that-disruption-of-ciliary-transition-zone-architecture-causes-joubert-syndrome
#15
Xiaoyu Shi, Galo Garcia, Julie C Van De Weghe, Ryan McGorty, Gregory J Pazour, Dan Doherty, Bo Huang, Jeremy F Reiter
This corrects the article DOI: 10.1038/ncb3599.
October 31, 2017: Nature Cell Biology
https://www.readbyqxmd.com/read/29087382/reforms-spell-optimism-for-biological-research-in-china
#16
EDITORIAL
(no author information available yet)
No abstract text is available yet for this article.
October 31, 2017: Nature Cell Biology
https://www.readbyqxmd.com/read/28945232/extra-mitochondrial-prosurvival-bcl-2-proteins-regulate-gene-transcription-by-inhibiting-the-sufu%C3%A2-tumour-suppressor
#17
Xiaofeng Wu, Li-Shu Zhang, Jason Toombs, Yi-Chun Kuo, John Tyler Piazza, Rubina Tuladhar, Quinn Barrett, Chih-Wei Fan, Xuewu Zhang, Loren D Walensky, Marcel Kool, Steven Y Cheng, Rolf Brekken, Joseph T Opferman, Douglas R Green, Tudor Moldoveanu, Lawrence Lum
Direct interactions between pro- and anti-apoptotic BCL-2 family members form the basis of cell death decision-making at the outer mitochondrial membrane (OMM). Here we report that three anti-apoptotic BCL-2 proteins (MCL-1, BCL-2 and BCL-XL) found untethered from the OMM function as transcriptional regulators of a prosurvival and growth program. Anti-apoptotic BCL-2 proteins engage a BCL-2 homology (BH) domain sequence found in SUFU (suppressor of fused), a tumour suppressor and antagonist of the GLI DNA-binding proteins...
October 2017: Nature Cell Biology
https://www.readbyqxmd.com/read/28945231/insulin-fine-tunes-self-renewal-pathways-governing-naive-pluripotency-and-extra-embryonic-endoderm
#18
Kathryn G V Anderson, William B Hamilton, Fabian V Roske, Ajuna Azad, Teresa E Knudsen, Maurice A Canham, Lesley M Forrester, Joshua M Brickman
Signalling downstream of Activin/Nodal (ActA) and Wnt can induce endoderm differentiation and also support self-renewal in pluripotent cells. Here we find that these apparently contradictory activities are fine-tuned by insulin. In the absence of insulin, the combination of these cytokines supports endoderm in a context-dependent manner. When applied to naive pluripotent cells that resemble peri-implantation embryos, ActA and Wnt induce extra-embryonic primitive endoderm (PrE), whereas when applied to primed pluripotent epiblast stem cells (EpiSC), these cytokines induce gastrulation-stage embryonic definitive endoderm...
October 2017: Nature Cell Biology
https://www.readbyqxmd.com/read/28945230/cell-plasticity-in-epithelial-homeostasis-and-tumorigenesis
#19
REVIEW
Julia Varga, Florian R Greten
The adult organism is characterized by remarkable plasticity, which enables efficient regeneration and restoration of homeostasis after damage. When aberrantly activated, this plasticity contributes to tumour initiation and progression. Here we review recent advances in this field with a focus on cell fate changes and the epithelial-mesenchymal transition-two distinct, yet closely related, forms of plasticity with fundamental roles in homeostasis and cancer.
October 2017: Nature Cell Biology
https://www.readbyqxmd.com/read/28920955/mir-25-93-mediates-hypoxia-induced-immunosuppression-by-repressing-cgas
#20
Min-Zu Wu, Wei-Chung Cheng, Su-Feng Chen, Shin Nieh, Carolyn O'Connor, Chia-Lin Liu, Wen-Wei Tsai, Cheng-Jang Wu, Lorena Martin, Yaoh-Shiang Lin, Kou-Juey Wu, Li-Fan Lu, Juan Carlos Izpisua Belmonte
The mechanisms by which hypoxic tumours evade immunological pressure and anti-tumour immunity remain elusive. Here, we report that two hypoxia-responsive microRNAs, miR-25 and miR-93, are important for establishing an immunosuppressive tumour microenvironment by downregulating expression of the DNA sensor cGAS. Mechanistically, miR-25/93 targets NCOA3, an epigenetic factor that maintains basal levels of cGAS expression, leading to repression of cGAS during hypoxia. This allows hypoxic tumour cells to escape immunological responses induced by damage-associated molecular pattern molecules, specifically the release of mitochondrial DNA...
October 2017: Nature Cell Biology
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