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Bacillus subtilis strain deficient for the protein‐tyrosine kinase PtkA exhibits impaired DNA replication
Author(s) -
Petranovic Dina,
Michelsen Ole,
Zahradka Ksenija,
Silva Catarina,
Petranovic Mirjana,
Jensen Peter Ruhdal,
Mijakovic Ivan
Publication year - 2007
Publication title -
molecular microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.857
H-Index - 247
eISSN - 1365-2958
pISSN - 0950-382X
DOI - 10.1111/j.1365-2958.2007.05625.x
Subject(s) - biology , bacillus subtilis , strain (injury) , dna replication , replication (statistics) , microbiology and biotechnology , dna , bacteria , genetics , virology , anatomy
Summary Bacillus subtilis has recently come into the focus of research on bacterial protein‐tyrosine phosphorylation, with several proteins kinases, phosphatases and their substrates identified in this Gram‐positive model organism. B. subtilis protein‐tyrosine phosphorylation system PtkA/PtpZ was previously shown to regulate the phosphorylation state of UDP‐glucose dehydrogenases and single‐stranded DNA‐binding proteins. This promiscuity towards substrates is reminiscent of eukaryal kinases and has prompted us to investigate possible physiological effects of ptkA and ptpZ gene inactivations in this study. We were unable to identify any striking phenotypes related to control of UDP‐glucose dehydrogenases, natural competence and DNA lesion repair; however, a very strong phenotype of Δ ptkA emerged with respect to DNA replication and cell cycle control, as revealed by flow cytometry and fluorescent microscopy. B. subtilis cells lacking the kinase PtkA accumulated extra chromosome equivalents, exhibited aberrant initiation mass for DNA replication and an unusually long D period.