SHH (sonic hedgehog) encodes a glycoprotein involved in patterning and stem cell proliferation; it is required for patterning of the ventral neural tube, the anterior-posterior limb axis, and the ventral somites. SHH is also involved in differentiation of ventral forebrain neurons and midbrain dopaminergic neurons as well as proliferation and differentiation of cerebellar neuronal precursors. Impaired SHH signaling is associated with Down syndrome and neurodegenerative diseases. TRE-hShh knock-in mice express the dually lipidated fully active human sonic hedgehog (SHH) gene and a Zsgreen1 fluorescent reporter under the bidirectional tetracycline-responsive promoter (tetO). Mice homozygous for the allele are viable and fertile. When bred with another mouse expressing tetracycline-controlled transactivator protein (tTA - tet on) or reverse tetracycline-controlled transactivator protein (rtTA - tet off), tissue specific SHH expression in the resulting double positive offspring can be regulated with tetracycline or its analog doxycycline (dox). Activation of SHH expression also activates production of Zsgreen1 so that affected cells can be observed.
 When combined with mice carrying the forebrain specific Tg(Camk2a-tTA)1Mmay allele and a mouse model of Down syndrome (Ts65Dn - B6EiC3Sn.BLiA-Ts(1716)65Dn/DnJ), overexpression of SHH following tamoxifen administration in progeny results in normalized locomotor hyperactivity, improved learning and memory, reduced early onset cognitive impairment and enhance spatial cognition.

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These TRE-hShh knock-in mice express the human sonic hedgehog (SHH) gene and a Zsgreen1 fluorescent reporter, both regulated by the bidirectional tetracycline-responsive promoter (tetO). Tet-Off/Tet-On mutant mice provide conditional (inducible/reversible) expression of SHH and Zsgreen1 and maybe useful for studies of neurodegenerative disease.

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