Evidence map›Paper›PMID 30973898›Full record

ArticlePloS one2019

Mal3 is a multi-copy suppressor of the sensitivity to microtubule-depolymerizing drugs and chromosome mis-segregation in a fission yeast pka1 mutant.

Takuma Tanabe, Masayuki Yamaga, Makoto Kawamukai, Yasuhiro Matsuo

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Article in PloS one, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

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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

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3 · Its place in the literature

Who cites it

5 citing papers in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

4 authors.

Takuma TanabeDepartment of Life Sciences, Faculty of Life and Environmental Science, Shimane University, Matsue, Japan.
Masayuki YamagaDepartment of Life Sciences, Faculty of Life and Environmental Science, Shimane University, Matsue, Japan.
Makoto KawamukaiDepartment of Life Sciences, Faculty of Life and Environmental Science, Shimane University, Matsue, Japan.
Yasuhiro MatsuoDepartment of Life Sciences, Faculty of Life and Environmental Science, Shimane University, Matsue, Japan.ORCID 0000-0002-2858-7179

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The cAMP-dependent protein kinase Pka1 is known as a regulator of glycogenesis, transition into meiosis, chronological aging, and stress responses in the fission yeast, Schizosaccharomyces pombe. We demonstrated here that Pka1 is responsible for normal growth in the presence of the microtubule-destabilization drug TBZ and proper chromosome segregation. The deletion of the pka1 gene resulted in the TBZ-sensitive phenotype and chromosome mis-segregation. We isolated the mal3 gene as a multi-copy suppressor of the TBZ-sensitive phenotype in the pka1Δ strains. Overexpression of the CH domain (1-143) or the high-affinity microtubule binding mutant (1-143 Q89R) of Mal3 rescued the TBZ-sensitive phenotype in the pka1Δ and mal3Δ strains, while the EB1 domain (135-308) and the mutants defective in microtubule binding (1-143 Q89E) failed to do so in the same strains. Chromosome mis-segregation caused by TBZ in the pka1Δ or mal3Δ strains was suppressed by the overexpression of the Mal3 CH domain (1-143), Mal3 CH domain with the coiled-coil domain (1-197), or full-length Mal3. Overexpression of EB1 orthologs from Saccharomyces cerevisiae, Arabidopsis thaliana, Mus musculus, or Homo sapiens suppressed the TBZ-sensitive phenotype in the pka1Δ strains, indicating their conserved functions. These findings suggest that Pka1 and the microtubule binding of the Mal3 CH domain play a role in the maintenance of proper chromosome segregation.

Indexed as

AnimalsChromosome SegregationCyclic AMP-Dependent Protein KinasesGenes, FungalGenes, SuppressorHumansMiceMicrotubule-Associated ProteinsMicrotubulesMutationPhenotypeProtein DomainsSchizosaccharomycesSchizosaccharomyces pombe ProteinsTubulin ModulatorsCyclic AMP-Dependent Protein KinasesMal3 protein, S pombeMicrotubule-Associated ProteinsSchizosaccharomyces pombe ProteinsTubulin Modulators

Identifiers

PMID30973898
PMCPMC6459531

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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.