UV-mediated Chlamydomonas mutants with enhanced nuclear transgene expression by disruption of DNA methylation-dependent and independent silencing systems

UV-mediated Chlamydomonas mutants with enhanced nuclear transgene expression by disruption of DNA... Plant Mol Biol (2016) 92:629–641 DOI 19103-016-0510.1007/s1 -mediated UV Chlamydomonas mutants with enhanced nuclear transgene expression by disruption of DNA methylation- dependent and independent silencing systems 1 1 1 2 Sari Dewi Kurniasih · omohitoT amasakiY · Fantao Kong · Sigeru Okada · 1 1 Dwiyantari idyaningrumW · akeshiT Ohama Received: 14 May 2016 / Accepted: 10 August 2016 / Published online: 19 October 2016 © Springer Science +Business Media Dordrecht 2016 Abstract mechanisms involving MET1 , transgene expression is regu - Key message In this investigation, we succeeded to gen - lated by a DNA methylation-independent transgene silenc - erate mutants that bear dramatically ing system in Chlamydomonas . This is in agreement with enhanced ability for transgene expression. o yield these T the fact that DNA methylation occurs rarely in this ganor - mutants, we utilized DNA methyltransferase deficient ism. The generated mutants may be useful for the low-cost strain. These mutants must be useful as a plant cell factory. production of therapeutic proteins and eukaryotic enzymes Abstract Chlamydomonas rdtiieinhar (hereafter Chlam- based on their rapid growth in simple salt-based media. ydomonas ) is a green freshwater microalga. It is a promis - ing cell factory for http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Plant Molecular Biology Springer Journals

UV-mediated Chlamydomonas mutants with enhanced nuclear transgene expression by disruption of DNA methylation-dependent and independent silencing systems

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Publisher
Springer Netherlands
Copyright
Copyright © 2016 by Springer Science+Business Media Dordrecht
Subject
Life Sciences; Plant Sciences; Biochemistry, general; Plant Pathology
ISSN
0167-4412
eISSN
1573-5028
D.O.I.
10.1007/s11103-016-0529-9
Publisher site
See Article on Publisher Site

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