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  • Argonautes team up to silence transposable elements in Arabidopsis
    1. Charles J Underwood1 and
    2. Robert A Martienssen (martiens{at}cshl.edu) 1
    1. 1Howard Hughes Medical Institute‐Gordon and Betty Moore Foundation, Watson School of Biological Sciences, Cold Spring Harbor Laboratory, Cold Spring Harbor, NY, USA

    The de novo silencing of transposable elements in plants and animals is mediated in part by RNA‐directed chromatin modification. In flowering plants, AGO4 has been seen as the key argonaute protein in the RNA‐directed DNA methylation pathway that links the plant‐specific RNA polymerase V with the de novo DNA methyltransferase DRM2 (Zhong et al, 2014). Two recent papers in The EMBO Journal strongly implicate a role for the AGO6 protein in the process of de novo silencing.

    See also: C‐G Duan et al and

    AD McCue et al

    Two studies reveal that AGO6 cooperates with other argonaute proteins to silence transposable elements in plants.

    Charles J Underwood, Robert A Martienssen
  • Cross talk between ABC transporter mRNAs via a target mRNA‐derived sponge of the GcvB small RNA
    1. Masatoshi Miyakoshi1,
    2. Yanjie Chao1 and
    3. Jörg Vogel*,1
    1. 1RNA Biology Group, Institute for Molecular Infection Biology University of Würzburg, Würzburg, Germany
    1. *Corresponding author. Tel: +49 931 3182575; Fax: +49 931 3182578; E‐mail: joerg.vogel{at}uni-wuerzburg.de

    Decay of the bacterial GvcB sRNA, which keeps it from regulating its mRNA targets, is triggered by a 3′‐UTR‐derived fragment from a target mRNA. This ability of mRNAs to compete for regulatory RNA interaction presents a new mode of RNA cross talk in bacteria.

    Synopsis

    Decay of the bacterial GvcB sRNA, which keeps it from regulating its mRNA targets, is triggered by a 3′‐UTR‐derived fragment from a target mRNA. This ability of mRNAs to compete for regulatory RNA interaction presents a new mode of RNA cross talk in bacteria.

    • GcvB—a globally acting small regulatory RNA—is controlled by an RNA sponge

    • The stable mRNA breakdown fragment SroC destabilizes GcvB via RNase E

    • SroC is an RNA sponge that originates from one of GcvB's own target mRNAs

    • This finding provides evidence for a cross talk between ABC transporter mRNAs that involves SroC, GcvB, and Hfq

    • mRNA cross talk forms a new type of feed‐forward loop in a large regulatory RNA network

    .

    • GcvB
    • Hfq
    • noncoding RNA
    • RNase E
    • SroC
    • Received November 13, 2014.
    • Revision received December 12, 2014.
    • Accepted December 15, 2014.

    This is an open access article under the terms of the Creative Commons Attribution‐NonCommercial‐NoDerivs 4.0 License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made.

    Masatoshi Miyakoshi, Yanjie Chao, Jörg Vogel
  • CD19 and BAFF‐R can signal to promote B‐cell survival in the absence of Syk
    1. Elias Hobeika*,1,2,,
    2. Ella Levit‐Zerdoun1,,
    3. Vasiliki Anastasopoulou3,
    4. Roland Pohlmeyer1,
    5. Simon Altmeier4,
    6. Ameera Alsadeq5,
    7. Marc‐Werner Dobenecker6,
    8. Roberta Pelanda7 and
    9. Michael Reth*,1,2,8
    1. 1Max‐Planck Institute of Immunobiology and Epigenetics, Freiburg, Germany
    2. 2Department of Molecular Immunology, BioIII, Faculty of Biology, Albert‐Ludwigs‐Universität Freiburg, Freiburg, Germany
    3. 3Institute of Immunology, Charité Campus Buch, Berlin, Germany
    4. 4Institute of Mircobiology, Swiss Federal Institute of Technology, ETH Zurich, Zurich, Switzerland
    5. 5Department of General Pediatrics, University Medical Center Schleswig‐Holstein, Kiel, Germany
    6. 6Laboratory of Immune Cell Epigenetics and Signaling, The Rockefeller University, New York, NY, USA
    7. 7Department of Immunology and Microbiology, University of Colorado School of Medicine, Aurora, CO, USA
    8. 8BIOSS, Centre For Biological Signaling Studies, University of Freiburg, Freiburg, Germany
    1. * Corresponding author. Tel: +49 761 5108422; Fax: +49 761 5108423; E‐mail: hobeika{at}ie-freiburg.mpg.de

      Corresponding author. Tel: +49 761 5108420; Fax: +49 761 5108423; E‐mail: michael.reth{at}bioss.uni-freiburg.de

    1. These authors contributed equally to this work

    Syk‐deficient B cells require BAFF receptor and CD19/PI3K signaling for their long‐term survival and maintenance.

    Synopsis

    Survival of mature murine B cells primarily depends of signals from the BCR and BAFF‐R. Downstream of the BCR, the kinase Syk plays a pivotal role in the activation of various cell survival pathways including the PI3K pathway. Our in vivo experiments show that a considerable fraction of mature Syk‐negative B cells can survive however they require BAFF receptor and CD19/PI3K signaling for their long‐term maintenance.

    • A fraction of mature B cells (˜25%) can be maintained in the absence of the kinase Syk over a prolonged time frame in spite of defective BCR signaling and the inability to activate the mTORC1 pathway in response to BCR ligation.

    • This maintenance is dependent on signals from the BAFF receptor since blocking of BAFF—BAFF‐R interaction results in decreased numbers of Syk‐deficient B cells.

    • Furthermore, the expression of the BCR coreceptor CD19, which upon phosphorylation by Syk promotes PI3K activation, is required for the survival of Syk‐deficient B cells.

    • The viability of CD19; Syk double‐deficient B cells is restored by the conditional ablation of FoxO1, the latter mimicking hyperactive PI3K activation.

    • BAFF receptor
    • B‐cell antigen receptor
    • CD19
    • mb1‐CreERT2
    • Syk
    • Received August 6, 2014.
    • Revision received December 23, 2014.
    • Accepted January 2, 2015.
    Elias Hobeika, Ella Levit‐Zerdoun, Vasiliki Anastasopoulou, Roland Pohlmeyer, Simon Altmeier, Ameera Alsadeq, Marc‐Werner Dobenecker, Roberta Pelanda, Michael Reth
  • Wnt activity and basal niche position sensitize intestinal stem and progenitor cells to DNA damage
    1. Si Tao1,2,3,
    2. Duozhuang Tang1,
    3. Yohei Morita1,
    4. Tobias Sperka1,
    5. Omid Omrani1,
    6. André Lechel47,
    7. Vadim Sakk4,
    8. Johann Kraus5,
    9. Hans A Kestler1,5,
    10. Michael Kühl*,2 and
    11. Karl Lenhard Rudolph*,1,6
    1. 1Leibniz Institute for Age Research – Fritz Lipmann Institute e.V. (FLI), Jena, Germany
    2. 2Institute of Biochemistry and Molecular Biology, Ulm University, Ulm, Germany
    3. 3International Graduate School in Molecular Medicine Ulm, Ulm University, Ulm, Germany
    4. 4Cooperation Group between the Leibniz Institute for Age Research, Ulm University, Ulm, Germany
    5. 5Medical Systems Biology Unit, Ulm University, Ulm, Germany
    6. 6Research Group on Stem Cell Aging, Jena University Hospital (UKJ), Jena, Germany
    7. 7Department of Gastroenterology, University Hospital Ulm, Ulm, Germany
    1. * Corresponding author. Tel: +49 731 500 23283; Fax: +49 731 500 23277; E‐mail: michael.kuehl{at}uni-ulm.de

      Corresponding author. Tel: +49 3641 6563 50/52; Fax: +49 3641 6563 50/52; E‐mail: klrudolph{at}fli-leibniz.de

    New genetic results suggest that DNA damage‐induced modulation of Wnt signaling determines radio‐sensitivity of intestinal stem‐ and progenitor cells.

    Synopsis

    New genetic results suggest that DNA damage‐induced modulation of Wnt signaling determines radio‐sensitivity of intestinal stem‐ and progenitor cells.

    • Niche positioning‐associated Wnt signaling activity modulates sensitivity of intestinal stem and progenitor cells to DNA damage.

    • Wnt signaling enhances DNA damage responses in intestinal stem and progenitor cells.

    • Intestinal stem and progenitor cells with low Wnt activity preferentially survive in the context of DNA damage and telomere dysfunction.

    • Instructed enhancement of Wnt signaling increases radio‐sensitivity of intestinal stem and progenitor cells while inhibition of Wnt decreases it.

    • DNA damage
    • intestinal progenitor cells
    • intestinal stem cells
    • telomeres
    • Wnt
    • Received November 29, 2014.
    • Revision received December 22, 2014.
    • Accepted December 23, 2014.

    This is an open access article under the terms of the Creative Commons Attribution‐NonCommercial‐NoDerivs 4.0 License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made.

    Si Tao, Duozhuang Tang, Yohei Morita, Tobias Sperka, Omid Omrani, André Lechel, Vadim Sakk, Johann Kraus, Hans A Kestler, Michael Kühl, Karl Lenhard Rudolph
  • The mRNA decay factor PAT1 functions in a pathway including MAP kinase 4 and immune receptor SUMM2
    1. Milena Edna Roux1,,
    2. Magnus Wohlfahrt Rasmussen1,,
    3. Kristoffer Palma2,
    4. Signe Lolle1,
    5. Àngels Mateu Regué1,
    6. Gerit Bethke3,
    7. Jane Glazebrook3,
    8. Weiping Zhang4,
    9. Leslie Sieburth4,
    10. Martin R Larsen5,
    11. John Mundy1 and
    12. Morten Petersen*,1
    1. 1Department of Biology, Faculty of Science, University of Copenhagen, Copenhagen, Denmark
    2. 2New England Biolabs Ltd, Whitby, ON, Canada
    3. 3Department of Plant Biology, University of Minnesota, St. Paul, MN, USA
    4. 4Department of Biology, University of Utah, Salt Lake City, UT, USA
    5. 5University of Southern Denmark Institute for Biochemistry and Molecular Biology, Odense, Denmark
    1. *Corresponding author. Tel: +45 353 22127; E‐mail: shutko{at}bio.ku.dk
    1. These authors contributed equally to this work

    The identification of mRNA decapping factor PAT1 as a new target for MAP kinase 4 offers insight on the emerging connection between RNA metabolism and immunity in plants.

    Synopsis

    The identification of mRNA decapping factor PAT1 as a new target for MAP kinase 4 offers insight on the emerging connection between RNA metabolism and immunity in plants.

    • Eukaryotic PAT1 proteins are key components in post‐transcriptional regulation of gene expression

    • Arabidopsis PAT1 functions in decapping and is a substrate of MAP kinase 4 which regulates immune responses in a PAMP‐triggered pathway associated with the immune receptor SUMM2

    • PAT1 accumulates in processing (P) bodies upon PAMP treatment

    • PAT1 interacts with the resistance protein SUMM2 and pat1 mutants exhibit SUMM2‐dependent autoimmunity in Arabidopsis

    • decapping
    • immunity
    • MAP kinases
    • mRNA decay
    • phosphorylation
    • Received April 2, 2014.
    • Revision received December 2, 2014.
    • Accepted December 11, 2014.
    Milena Edna Roux, Magnus Wohlfahrt Rasmussen, Kristoffer Palma, Signe Lolle, Àngels Mateu Regué, Gerit Bethke, Jane Glazebrook, Weiping Zhang, Leslie Sieburth, Martin R Larsen, John Mundy, Morten Petersen
  • miR‐290/371‐Mbd2‐Myc circuit regulates glycolytic metabolism to promote pluripotency
    1. Yang Cao1,,
    2. Wen‐Ting Guo2,,
    3. Shengya Tian1,
    4. Xiaoping He1,
    5. Xi‐Wen Wang2,
    6. Xiaomeng Liu3,
    7. Kai‐Li Gu2,
    8. Xiaoyu Ma1,
    9. De Huang1,
    10. Lan Hu1,
    11. Yongping Cai4,
    12. Huafeng Zhang1,
    13. Yangming Wang*,2 and
    14. Ping Gao*,1
    1. 1The CAS Key Laboratory of Innate Immunity and Chronic Disease, Innovation Center for Cell Biology, School of Life Sciences, University of Science and Technology of China, Hefei, China
    2. 2Beijing Key Laboratory of Cardiometabolic Molecular Medicine, Peking‐Tsinghua Center for Life Sciences, Institute of Molecular Medicine, Peking University, Beijing, China
    3. 3Biodynamic Optical Imaging Center, College of Life Sciences, Peking University, Beijing, China
    4. 4Department of Pathology, School of Medicine, Anhui Medical University, Hefei, China
    1. * Corresponding author. Tel: +86 10 62766945; E‐mail: yangming.wang{at}pku.edu.cn

      Corresponding author. Tel: +86 551 63607033; E‐mail: pgao2{at}ustc.edu.cn

    1. These authors contributed equally to this work

    New data reveal a miRNA‐Mbd2‐Myc network that directly controls metabolic enzymes to govern stem cell metabolism and pluripotency.

    Synopsis

    New data reveal a miRNA‐Mbd2‐Myc network that directly controls metabolic enzymes to govern stem cell metabolism and pluripotency.

    • miR‐290 cluster stimulates glycolytic metabolism to promote pluripotency.

    • miR‐290 cluster targets Mbd2 that represses glycolysis and reprogramming.

    • Mbd2 suppresses Myc that is critical for metabolic switch in ESCs.

    • miR‐371 cluster stimulates glycolysis to promote human somatic cell reprogramming.

    • glycolysis
    • microRNA
    • Mbd2
    • metabolism
    • pluripotency
    • Received October 30, 2014.
    • Revision received December 19, 2014.
    • Accepted December 23, 2014.
    Yang Cao, Wen‐Ting Guo, Shengya Tian, Xiaoping He, Xi‐Wen Wang, Xiaomeng Liu, Kai‐Li Gu, Xiaoyu Ma, De Huang, Lan Hu, Yongping Cai, Huafeng Zhang, Yangming Wang, Ping Gao
  • Progesterone and Wnt4 control mammary stem cells via myoepithelial crosstalk
    1. Renuga Devi Rajaram15,
    2. Duje Buric1,
    3. Marian Caikovski1,
    4. Ayyakkannu Ayyanan1,
    5. Jacques Rougemont2,
    6. Jingdong Shan3,
    7. Seppo J Vainio3,
    8. Ozden Yalcin‐Ozuysal4 and
    9. Cathrin Brisken*,1
    1. 1Ecole Polytechnique Fédérale de Lausanne (EPFL) ISREC ‐ Swiss Institute for Experimental Cancer Research, Lausanne, Switzerland
    2. 2Swiss Institute of Bioinformatics Bioinformatics and Biostatistics Core Facility Ecole polytechnique fédérale de Lausanne (EPFL), Lausanne, Switzerland
    3. 3Faculty of Biochemisty and Molecular Medicine (FBMM), Biocenter Oulu and Infotech Oulu Oulu Center for Cell Matrix Research University of Oulu, Oulu, Finland
    4. 4Department of Molecular Biology and Genetics, Izmir Institute of Technology, Izmir, Turkey
    5. 5Department of Pharmacology and Toxicology, University of Lausanne, Lausanne, Switzerland
    1. *Corresponding author. Tel +41 21 693 07 81; +41 21 693 07 62; Fax +41 21 693 07 40; E‐mail: cathrin.brisken{at}epfl.ch

    This paper ascribes a new role for Wnt4 in pre‐pubertal mammary gland development while revealing luminal cells to respond to Wnt activation. During regeneration, Wnt4 interacts with progesterone receptor signaling, correcting previous notions on RANKL signaling in this context.

    Synopsis

    This paper ascribes a new role for Wnt4 in pre‐pubertal mammary gland development while revealing luminal cells to respond to Wnt activation. During regeneration, Wnt4 interacts with progesterone receptor signaling, correcting previous notions on RANKL signaling in this context.

    • Wnt4 is an essential control factor for mammary epithelial stem cell function.

    • RANKL is not required for mammary gland regeneration potential.

    • Wnt4 activates canonical Wnt signaling in the basal/myoepithelial compartment.

    • Progesterone receptor signaling is required for mammary epithelial Wnt4 expression already during puberty.

    • canonical Wnt signaling
    • hormones
    • mammary stem cells
    • myoepithelium
    • paracrine
    • Received October 30, 2014.
    • Revision received December 21, 2014.
    • Accepted December 23, 2014.
    Renuga Devi Rajaram, Duje Buric, Marian Caikovski, Ayyakkannu Ayyanan, Jacques Rougemont, Jingdong Shan, Seppo J Vainio, Ozden Yalcin‐Ozuysal, Cathrin Brisken