Cdh5-Opto&alpha;1AR-IRES-lacZ transgenic mice express the light-sensitive Opto&alpha;1AR fusion protein and lacZ under control of the Cdh5 locus promoter/enhancer regions within the BAC transgene. Cdh5-Opto&alpha;1AR-IRES-lacZ mice from founder line B26-1 exhibit high expression levels of Opto&alpha;1AR and lacZ in vascular endothelial cells (e.g., heart, lung, brain) - consistent with endogenous Cdh5. Additional details described further below. The Opto&alpha;1AR fusion protein has the transmembrane and light-sensitive domains from bovine G protein-coupled protein rhodopsin with the intracellular domains from human &alpha;1a-adrenergic receptor (ADRA1A). When activated with light (~473 nm), Opto&alpha;1AR generates the secondary messengers IP3 and diacylglycerol (DAG). For Cdh5-Opto&alpha;1AR-IRES-lacZ transgenic mice, light activation of the Opto&alpha;1AR molecule in endothelial cells in blood vessels results in increased levels of cytoplasmic IP3/DAG - which causes a cascade reaction, calcium release, calcium signaling and dilation of overlying smooth muscle.
 The donating investigator reports that expression patterns appear to mimic the endogenous Cdh5 expression. Specifically, lacZ staining (after harvesting and staining tissues) was observed in blood vessel endothelial cells of the heart, brain and lung, as well as in vascular endothelial cells of cremaster muscle and femoral artery. They have not tested expression in other tissues to date (March 2019). Before exposure to the specific wavelength of activating light, lacZ expression is observable (after harvesting and staining tissues), and the Opto&alpha;1AR imparts no IP3/DAG release and no endothelial changes. Upon exposure to ~473 nm light, Opto&alpha;1AR activation releases IP3/DAG - which causes a cascade reaction, calcium release, calcium signaling and dilation of overlying smooth muscle. Subsequent removal of the activating light returns overlying smooth muscle to the baseline state. Mice hemizygous for the Cdh5-Opto&alpha;1AR-IRES-lacZ transgene are viable and fertile with normal breeding, and no reported gross phenotypic abnormalities. To date (March 2019), it has not been attempted to make this strain homozygous. This mouse model is available by way of a collaborative effort between Cornell/National Heart Lung Blood Resource for Optogenetic Mouse Signaling (<a href="http://chromus.vet.cornell.edu">CHROMus</a>) and The Jackson Laboratory.

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Cdh5-Opto&alpha;1AR-IRES-lacZ transgenic mice express the light-sensitive effector protein Opto&alpha;1AR in vascular endothelial cells (e.g., heart, lung, brain). Light activation of the Opto&alpha;1AR molecule in endothelial cells in blood vessels results in increased levels of cytoplasmic IP3 and diacylglycerol (DAG) - which causes a cascade reaction, calcium release, calcium signaling and dilation of overlying smooth muscle.

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