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Scientific DataVolume 2, 12 May 2015, Article number 201520

Genome-wide RNAi screen for synthetic lethal interactions with the C. elegans kinesin-5 homolog BMK-1(Article)(Open Access)

  • Maia, A.F.,
  • Tanenbaum, M.E.,
  • Galli, M.,
  • Lelieveld, D.,
  • Egan, D.A.,
  • Gassmann, R.,
  • Sunkel, C.E.,
  • Van Den Heuvel, S.,
  • Medema, R.H.
  • View Correspondence (jump link)
  • aInstituto de Investigação e Inovação em Saúde, Universidade do Porto, Porto, Portugal
  • bDepartment of Medical Oncology, Laboratory of Experimental Oncology, University Medical Center Utrecht, Utrecht, 3584 CG, Netherlands
  • cDevelopmental Biology, Utrecht University, Utrecht, 3584 CH, Netherlands
  • dDepartment of Cell Biology, Cell Microscopy Center, University Medical Center Utrecht, Utrecht, 3584 CX, Netherlands
  • eInstituto de Biologia Molecular e Celular, Universidade do Porto, Rua do Campo Alegre 823, Porto, 4150-180, Portugal
  • fDepartment of Cellular and Molecular Pharmacology, University of California San Francisco, San Francisco, California 94158-2140, United States
  • gDepartment of Physiology, University of California San Francisco, San Francisco, California 94143, United States
  • hDepartment of Cell Biology, Netherlands Cancer Institute, Amsterdam, 1006 BE, Netherlands

Abstract

Kinesins are a superfamily of microtubule-based molecular motors that perform various transport needs and have essential roles in cell division. Among these, the kinesin-5 family has been shown to play a major role in the formation and maintenance of the bipolar mitotic spindle. Moreover, recent work suggests that kinesin-5 motors may have additional roles. In contrast to most model organisms, the sole kinesin-5 gene in Caenorhabditis elegans, bmk-1, is not required for successful mitosis and animals lacking bmk-1 are viable and fertile. To gain insight into factors that may act redundantly with BMK-1 in spindle assembly and to identify possible additional cellular pathways involving BMK-1, we performed a synthetic lethal screen using the bmk-1 deletion allele ok391. We successfully knocked down 82% of the C. elegans genome using RNAi and assayed viability in bmk-1(ok391) and wild type strains using an automated high-throughput approach based on fluorescence microscopy. The dataset includes a final list of 37 synthetic lethal interactions whose further study is likely to provide insight into kinesin-5 function.

Indexed keywords

EMTREE drug terms:Caenorhabditis elegans proteinkinesinmicrotubule associated protein
EMTREE medical terms:animalCaenorhabditis elegansgeneticsgenomelethal genemetabolismRNA interferencesignal transductionspindle apparatus
MeSH:AnimalsCaenorhabditis elegansCaenorhabditis elegans ProteinsGenes, LethalGenome, HelminthKinesinMicrotubule-Associated ProteinsRNA InterferenceSignal TransductionSpindle Apparatus

Chemicals and CAS Registry Numbers:

Caenorhabditis elegans Proteins; Kinesin; Microtubule-Associated Proteins

  • ISSN: 20524463
  • Source Type: Journal
  • Original language: English
  • DOI: 10.1038/sdata.2015.20
  • PubMed ID: 25984351
  • Document Type: Article
  • Publisher: Nature Publishing Groups

  Medema, R.H.; Department of Cell Biology, Netherlands Cancer Institute, Amsterdam, Netherlands;
© Copyright 2016 Elsevier B.V., All rights reserved.

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