S
Sota Hiraga
Researcher at Kumamoto University
Publications - 57
Citations - 5233
Sota Hiraga is an academic researcher from Kumamoto University. The author has contributed to research in topics: Mutant & Escherichia coli. The author has an hindex of 33, co-authored 57 publications receiving 5082 citations. Previous affiliations of Sota Hiraga include University of Edinburgh.
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Journal ArticleDOI
New topoisomerase essential for chromosome segregation in E. coli
TL;DR: It is suggested that the parC and parE genes code for the subunits of a new topoisomerase, named topo IV.
Journal ArticleDOI
Mini-F plasmid genes that couple host cell division to plasmid proliferation.
Teru Ogura,Sota Hiraga +1 more
TL;DR: Experimental results suggest that reduction of the copy number of plasmids carrying the ccd region causes an inhibition of cell division and that the cccd region can be dissected into two functional regions; one (ccdB) inhibits celldivision and the other (ccdA) releases the inhibition.
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The new gene mukB codes for a 177 kd protein with coiled-coil domains involved in chromosome partitioning of E. coli.
TL;DR: The isolated Escherichia coli temperature sensitive mutant, named mukB, is defective in a previously undescribed gene and the absence of MukB leads to aberrant chromosome partitioning.
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Chromosome partitioning in Escherichia coli: novel mutants producing anucleate cells.
TL;DR: Results suggest that the mutant is defective in the chromosome positioning at regular intracellular positions and fails frequently to partition the replicated daughter chromosomes into both daughter cells, resulting in production of one anucleate daughter cell and one with two chromosomes.
Chromosome Partitioning inEscherichia coli: NovelMutants Producing Anucleate Cells
TL;DR: In this article, the authors have isolated a type of Escherichia coli mutants which formed anucleate cells, named mukA1, by using newly developed techniques and found that the mutant is defective in the chromosome positioning at regular intracellular positions and fails frequently to partition the replicated daughter chromosomes into both daughter cells.