The Bacillus subtilis essential gene dgkB is dispensable in mutants with defective lipoteichoic acid synthesis
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- Matsuoka Satoshi
- Department of Biochemistry and Molecular Biology, Graduate School of Science and Engineering, Saitama University
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- Hashimoto Michihiro
- Department of Biochemistry and Molecular Biology, Graduate School of Science and Engineering, Saitama University
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- Kamiya Yusuke
- Department of Biochemistry and Molecular Biology, Graduate School of Science and Engineering, Saitama University
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- Miyazawa Takeshi
- Department of Biochemistry and Molecular Biology, Graduate School of Science and Engineering, Saitama University
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- Ishikawa Kazuki
- Department of Biochemistry and Molecular Biology, Graduate School of Science and Engineering, Saitama University
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- Hara Hiroshi
- Department of Biochemistry and Molecular Biology, Graduate School of Science and Engineering, Saitama University
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- Matsumoto Kouji
- Department of Biochemistry and Molecular Biology, Graduate School of Science and Engineering, Saitama University
書誌事項
- タイトル別名
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- The <i>Bacillus subtilis</i> essential gene <i>dgkB</i> is dispensable in mutants with defective lipoteichoic acid synthesis
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抄録
The dgkB gene is essential for the growth of Bacillus subtilis. It encodes a diacylglycerol (DG) kinase that converts DG to phosphatidic acid to reintroduce it into the phospholipid synthesis pathway. Repression of the dgkB gene placed under a regulatable promoter causes accumulation of DG and leads to lethality. DG is formed as a byproduct of the synthesis of lipoteichoic acid (LTA), a polyanionic component of the cell envelope. B. subtilis synthesizes LTA by polymerizing the glycerophosphate moiety of phosphatidylglycerol (PG) onto a glucolipid membrane anchor, and releasing the DG moiety of PG. B. subtilis has four genes homologous to Staphylococcus aureus ltaS, which encodes LTA synthase. Disruption of either or both of two genes, yflE and yfnI, whose products show higher homology with S. aureus LtaS among the four homologues, suppressed the lethality caused by dgkB repression. In cells with dgkB repression, DG was accumulated to 43 ± 3% of total lipids, about three times the content of wild type cells (13 ± 1%). Disruption of yfnI in the dgkB-repressed cells reduced the DG content to 15 ± 2%, but yflE-disruption did not (42 ± 1%); this was probably due to efficient LTA synthesis by YfnI in the yflE-disrupted cells. Further introduction of a disrupted allele of ugtP, encoding glucolipid synthase that consumes DG as a substrate, partially lowered the colony forming capacity in strains with yflE-disruption. A disrupted dgkB allele was successfully introduced into strains disrupted for either or both of yflE and yfnI, indicating that the essential gene dgkB is dispensable in mutants defective in LTA synthesis.<br>
収録刊行物
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- Genes & Genetic Systems
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Genes & Genetic Systems 86 (6), 365-376, 2011
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詳細情報 詳細情報について
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- CRID
- 1390282680451488256
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- NII論文ID
- 10030210125
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- NII書誌ID
- AA11077421
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- COI
- 1:STN:280:DC%2BC38vpvVOnsA%3D%3D
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- ISSN
- 18805779
- 13417568
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- NDL書誌ID
- 023513490
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- PubMed
- 22451476
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- 本文言語コード
- en
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- データソース種別
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- JaLC
- NDL
- Crossref
- PubMed
- CiNii Articles
- KAKEN
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- 抄録ライセンスフラグ
- 使用不可