Evidence map›Paper›PMID 25984351›Full record

ArticleScientific data2015

Genome-wide RNAi screen for synthetic lethal interactions with the C. elegans kinesin-5 homolog BMK-1.

André F Maia, Marvin E Tanenbaum, Matilde Galli, Daphne Lelieveld, David A Egan, Reto Gassmann, Claudio E Sunkel, Sander van den Heuvel, René H Medema

Open access · goldAbstract readDataset
In one paragraph

Article in Scientific data, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.9field-weighted citation impact, top 26% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

9 citing papers in PubMed, 12 citations in OpenAlex.

  1. Article
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  3. Yolk-deprivedLife science alliance · 2023
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors at 3 institutions in 2 countries.

André F MaiaInstituto de Investigação e Inovação em Saúde, Universidade do Porto , Porto, Portugal ; Department of Medical Oncology, Laboratory of Experimental Oncology, University Medical Center Utrecht , 3584 CG Utrecht, The Netherlands.
Marvin E TanenbaumDepartment of Medical Oncology, Laboratory of Experimental Oncology, University Medical Center Utrecht , 3584 CG Utrecht, The Netherlands.
Matilde GalliDevelopmental Biology, Utrecht University , 3584 CH Utrecht, The Netherlands.
Daphne LelieveldDepartment of Cell Biology, Cell Microscopy Center, University Medical Center Utrecht , 3584 CX Utrecht, The Netherlands.
David A EganDepartment of Cell Biology, Cell Microscopy Center, University Medical Center Utrecht , 3584 CX Utrecht, The Netherlands.
Reto GassmannInstituto de Investigação e Inovação em Saúde, Universidade do Porto , Porto, Portugal.
Claudio E SunkelInstituto de Investigação e Inovação em Saúde, Universidade do Porto , Porto, Portugal.
Sander van den HeuvelDevelopmental Biology, Utrecht University , 3584 CH Utrecht, The Netherlands.
René H MedemaDepartment of Medical Oncology, Laboratory of Experimental Oncology, University Medical Center Utrecht , 3584 CG Utrecht, The Netherlands.
University Medical Center Utrecht · NLi3S - Instituto de Investigação e Inovação em Saúde, Universidade do Porto · PTUtrecht University · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

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 as

Caenorhabditis elegansCaenorhabditis elegans ProteinsKinesinsMicrotubule-Associated ProteinsAnimalsGenes, LethalGenome, HelminthRNA InterferenceSignal TransductionSpindle ApparatusCaenorhabditis elegans ProteinsKinesinsMicrotubule-Associated Proteins

Identifiers

PMID25984351
PMCPMC4431526
OpenAlexW2275300921

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.