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. 2017 Aug 23;7:9195. doi: 10.1038/s41598-017-09697-x

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© The Author(s) 2017

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Schematic principle and system design of photo-control over specific oncogene expression. (A) A protein (Prot) of interest genetically fused with the estrogen receptor (ERT2) is inactivated by the complex it forms with cytoplasmic chaperones (hsp). This complex can be dissociated by binding of a specific inducer (e.g. cyclofen) to ERT2. (B) A caged inducer (caged cyclofen, cInd) is chemically synthesized and can be uncaged by illumination at ~370 nm (~740 nm with a two-photon source). (C) The scheme describes how the expression of an oncogene can be photo-activated in a live cell transfected with dual fluorescent markers (EosFP and CFP). (D) This example shows that expression of the oncogene was induced selectively in one muscle fiber cell through localized uncaging of cInd in a developing zebrafish embryo. The injected embryo mosaically expressed EosFP, but only the light-activated cell expressed CFP (arrow denoted). (E,F) Two systems were used to control the transient or constitutive expression of kRASG12V. Scale bar: 200 μm.