2010年5月
Enhancement of beta-glucosidase activity on the cell-surface of sake yeast by disruption of SED1
JOURNAL OF BIOSCIENCE AND BIOENGINEERING
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- 巻
- 109
- 号
- 5
- 開始ページ
- 442
- 終了ページ
- 446
- 記述言語
- 英語
- 掲載種別
- 研究論文(学術雑誌)
- DOI
- 10.1016/j.jbiosc.2009.11.003
- 出版者・発行元
- SOC BIOSCIENCE BIOENGINEERING JAPAN
We determined the genetic background that would result in a more optimal display of heterologously expressed p-glucosidase (BGL) on the cell surface of yeast Saccharomyces cerevisiae. Amongst a collection of 28 strains carrying deletions in genes for glycosylphosphatidyl inositol (GPI)-anchored proteins, the Delta sed1 and Delta tos6 strains had significantly higher BGL-activity whilst maintaining wild type growth. Absence of Sed1p, which might facilitate incorporation of anchored BGL on the cell-surface, could also influence the activity of BGL on the cell surface with the heterologous gene being placed under the control of the SED1 promoter. For the evaluation of its industrial applicability we tested this system in heterologous and homogenous SED1-disruptants of sake yeast, a diploid S. cerevisiae strain, in which either the SED1 ORF or the complete gene including the promoter was deleted by use of the high-efficiency loss of heterozygosity method. Evaluation of disruptants displaying BGL showed that deletion of the SED1 ORF enhanced BGL activity on the cell surface, while additional deletion of the SED1 promoter increased further BGL activity on the cell surface. Compared to heterozygous disruption, homozygous disruption resulted generally in a higher BGL activity. Thus, homozygous deletion of both SED1 gene and promoter resulted in the most efficient display of BGL reaching a 1.6-fold increase of BGL-activity compared to wild type. (C) 2009, The Society for Biotechnology, Japan. All rights reserved.
- リンク情報
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- DOI
- https://doi.org/10.1016/j.jbiosc.2009.11.003
- J-GLOBAL
- https://jglobal.jst.go.jp/detail?JGLOBAL_ID=201002249382022069
- CiNii Articles
- http://ci.nii.ac.jp/naid/110007618918
- Web of Science
- https://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=JSTA_CEL&SrcApp=J_Gate_JST&DestLinkType=FullRecord&KeyUT=WOS:000279089600003&DestApp=WOS_CPL
- ID情報
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- DOI : 10.1016/j.jbiosc.2009.11.003
- ISSN : 1389-1723
- eISSN : 1347-4421
- J-Global ID : 201002249382022069
- CiNii Articles ID : 110007618918
- Web of Science ID : WOS:000279089600003