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Gli2 is required for induction of floor plate and adjacent cells, but not most ventral neurons in the mouse central nervous system.
It is found that the floor plate throughout the midbrain, hindbrain and spinal cord does not form in Gli2 homozygotes, suggesting that early signals derived from the notochord can be sufficient for establishing the basic d/v domains of cell differentiation in the ventral spinal cord and hindbrain.
A role for Gbx2 in repression of Otx2 and positioning the mid/hindbrain organizer
It is proposed that formation of a normal MHB organizer depends on a sharp Otx2 caudal border and that Gbx2 is required to position and sharpen this border.
Specification of the mammalian cochlea is dependent on Sonic hedgehog.
Sonic hedgehog secreted by the notochord and/or floor plate is identified as a primary regulator of auditory cell fates within the mouse inner ear and data support a model whereby auditory cellfates in the otic vesicle are established by the direct action of Shh.
Wnt-dependent regulation of inner ear morphogenesis is balanced by the opposing and supporting roles of Shh.
It is demonstrated that Wnt signaling is active in dorsal regions of the otic vesicle, where it functions to regulate the expression of genes necessary for vestibular morphogenesis.
Regionalization of Sonic hedgehog transcription along the anteroposterior axis of the mouse central nervous system is regulated by Hnf3-dependent and -independent mechanisms.
The results support the existence of Hnf3-dependent and -independent mechanisms in the direct activation of Shh transcription within the CNS and axial mesoderm.
A functional screen for sonic hedgehog regulatory elements across a 1 Mb interval identifies long-range ventral forebrain enhancers
An enhancer trap assay was devised to systematically screen 1 Mb of DNA surrounding the Shh locus for the ability to target reporter gene expression to sites of Shh transcription in transgenic mouse embryos, uncovering six enhancers distributed over 400 kb that regulated Shh-like expression in the ventral midbrain, the majority of the ventralsidephalon and parts of the telencephalon.