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  • Review
    ESCRTs are everywhere
    ESCRTs are everywhere
    1. James H Hurley*,1,2
    1. 1Department of Molecular and Cell Biology and California Institute for Quantitative Biosciences, University of California, Berkeley, Berkeley, CA, USA
    2. 2Life Sciences Division, Lawrence Berkeley National Lab, Berkeley, CA, USA
    1. *Corresponding author. E‐mail: jimhurley{at}berkeley.edu

    ESCRT complexes are required for membrane remodeling and scission; this review highlights their role in cellular processes ranging from exosome generation to the reformation of the nuclear envelope.

    • exosome
    • exovesicle
    • nuclear envelope reformation
    • plasma membrane wound repair
    • shedding microvesicle
    • Received July 7, 2015.
    • Revision received July 27, 2015.
    • Accepted July 30, 2015.
    James H Hurley
  • Article
    RuvbL1 and RuvbL2 enhance aggresome formation and disaggregate amyloid fibrils
    RuvbL1 and RuvbL2 enhance aggresome formation and disaggregate amyloid fibrils
    1. Nava Zaarur1,
    2. Xiaobin Xu2,
    3. Patrick Lestienne3,
    4. Anatoli B Meriin1,
    5. Mark McComb2,
    6. Catherine E Costello1,2,
    7. Gary P Newnam4,
    8. Rakhee Ganti4,
    9. Nina V Romanova5,
    10. Maruda Shanmugasundaram6,
    11. Sara TN Silva7,
    12. Tiago M Bandeiras8,
    13. Pedro M Matias7,8,
    14. Kirill S Lobachev4,
    15. Igor K Lednev6,
    16. Yury O Chernoff*,4,5 and
    17. Michael Y Sherman*,1
    1. 1Department of Biochemistry, Boston University School of Medicine, Boston, MA, USA
    2. 2Center for Biomedical Mass Spectrometry, Boston University School of Medicine, Boston, MA, USA
    3. 3INSERM U 1053, University of Bordeaux Segalen, Bordeaux, France
    4. 4School of Biology, Georgia Institute of Technology, Atlanta, GA, USA
    5. 5Laboratory of Amyloid Biology and Institute of Translational Biomedicine, St. Petersburg State University, St. Petersburg, Russia
    6. 6Department of Chemistry, University at Albany, State University of New York, Albany, NY, USA
    7. 7Instituto de Tecnologia Química e Biológica António Xavier, Universidade Nova de Lisboa, Oeiras, Portugal
    8. 8Instituto de Biologia Experimental e Tecnológica, Oeiras, Portugal
    1. * Corresponding author. Tel: +1 404 894 1157; E‐mail: yury.chernoff{at}biology.gatech.edu

      Corresponding author. Tel: +1 617 638 5971; E‐mail: sherma1{at}bu.edu

    The AAA+ ATPase RuvbL is required for aggresome formation and serves as a protein disaggregase that can disassemble amyloids in mammalian and yeast cells.

    Synopsis

    The AAA+ ATPase RuvbL is required for aggresome formation and serves as a protein disaggregase that can disassemble amyloids in mammalian and yeast cells.

    • Depletion of AAA+ ATPases RuvbL1 or RuvbL2 enhances aggregation of certain proteins in mammalian cells and inhibits aggresome formation.

    • RuvbL directly interacts with aggresome substrates, and the site of interaction is in the proximity to the internal channel of its barrel‐like structure.

    • Purified RuvbL inhibits seeding and promotes fragmentation of amyloid fibrils.

    • RuvbL depletion slows down disassembly of protein aggregates in mammalian cells and enhances proteotoxicity.

    • In yeast, RuvbL orthologs protect from heat shock and protein toxicity independently of Hsp104.

    • aggresome
    • amyloid
    • disaggregation
    • RuvbL
    • Received February 10, 2015.
    • Revision received July 9, 2015.
    • Accepted July 13, 2015.
    Nava Zaarur, Xiaobin Xu, Patrick Lestienne, Anatoli B Meriin, Mark McComb, Catherine E Costello, Gary P Newnam, Rakhee Ganti, Nina V Romanova, Maruda Shanmugasundaram, Sara TN Silva, Tiago M Bandeiras, Pedro M Matias, Kirill S Lobachev, Igor K Lednev, Yury O Chernoff, Michael Y Sherman
  • Corrigendum
    Differential effects of viral silencing suppressors on siRNA and miRNA loading support the existence of two distinct cellular pools of ARGONAUTE1
    Differential effects of viral silencing suppressors on siRNA and miRNA loading support the existence of two distinct cellular pools of ARGONAUTE1
    Gregory Schott, Arturo Mari‐Ordonez, Christophe Himber, Abdelmalek Alioua, Olivier Voinnet, Patrice Dunoyer
  • Corrigendum
    Nuclear import of CaMV P6 is required for infection and suppression of the RNA silencing factor DRB4
    Nuclear import of CaMV P6 is required for infection and suppression of the RNA silencing factor DRB4
    Gabrielle Haas, Jacinthe Azevedo, Guillaume Moissiard, Angèle Geldreich, Christophe Himber, Marina Bureau, Toshiyuki Fukuhara, Mario Keller, Olivier Voinnet
  • Corrigendum
    Two classes of short interfering RNA in RNA silencing
    Andrew Hamilton, Olivier Voinnet, Louise Chappell, David Baulcombe
  • Article
    Polynucleotide kinase–phosphatase enables neurogenesis via multiple DNA repair pathways to maintain genome stability
    Polynucleotide kinase–phosphatase enables neurogenesis via multiple DNA repair pathways to maintain genome stability
    1. Mikio Shimada12,
    2. Lavinia C Dumitrache1,
    3. Helen R Russell1 and
    4. Peter J McKinnon*,1
    1. 1Department of Genetics, St Jude Children's Research Hospital, Memphis, TN, USA
    2. 2Tokyo Institute of Technology, Tokyo, Japan
    1. *Corresponding author. Tel: +1 901 595 2700; Fax: +1 901 595 6035; E‐mail: peter.mckinnon{at}stjude.org

    Polynucleotide kinase‐phosphatase is essential for normal brain development by preventing the accumulation of endogenous DNA single‐ and double‐strand breaks, which otherwise results in widespread cell death during neurogenesis.

    Synopsis

    Polynucleotide kinase‐phosphatase (PNKP), a repair factor that modifies DNA breaks prior to ligation, is essential for normal brain development by preventing the accumulation of endogenous DNA breaks, which otherwise results in widespread cell death during neurogenesis.

    • PNKP is essential for neurogenesis by preventing DNA damage accumulation.

    • PNKP is required for efficient base‐excision repair (BER) of single‐strand breaks as well as non‐homologous end joining (NHEJ) repair of double‐strand breaks.

    • Attenuated PNKP levels generated using a hypomorphic Pnkp allele compromised brain development and generate a microcephaly with seizures (MCSZ)‐like neural phenotype.

    • Postnatal inactivation of PNKP in various neural compartments resulted in defective cellular homeostasis in mature cell types in the brain, including select neurons and oligodendrocytes.

    • DNA repair
    • neurodevelopment
    • neurologic disease
    • polynucleotide kinase–phosphatase
    • Received February 23, 2015.
    • Revision received June 19, 2015.
    • Accepted July 9, 2015.
    Mikio Shimada, Lavinia C Dumitrache, Helen R Russell, Peter J McKinnon
  • Retraction
    Retraction: ‘An endogenous, systemic RNAi pathway in plants’
    Patrice Dunoyer, Christopher A Brosnan, Gregory Schott, Yu Wang, Florence Jay, Abdelmalek Alioua, Christophe Himber, Olivier Voinnet