High impact information on gli2a

• Using a comparative synteny approach, we isolated yot as a zinc finger transcription factor homologous to the Hh target gli2 [1].
• Zebrafish you-too (yot) mutations interfere with Hedgehog (Hh) signaling during embryogenesis [1].
• In addition to causing defects in midline development, muscle differentiation, and retinal axon guidance, yot mutations disrupt anterior pituitary and ventral forebrain differentiation. yot mutations also cause ectopic lens formation in the ventral diencephalon [1].
• To clarify the roles of gli genes during vertebrate development, we have analyzed the requirements for gli1 and gli2 during zebrafish embryogenesis [2].
• However, gli2 knockdown in wild-type embryos generated no discernable motor neuron phenotype, while gli3 knockdown reduced motor neuron induction in the hindbrain and spinal cord [3].

Biological context of gli2a

• Indeed, morpholino-mediated knockdown of Gli2(DR) protein in yot mutants led to a suppression of the defective motor neuron phenotype [3].
• Two yot mutant alleles with midline lenses likely encode dominant negative forms of the Gli2 protein which will interfere with transcriptional activation by other Gli proteins [4].
• We report here the characterization of a zebrafish Gli2 expression in slow and fast muscle cells and the study of the roles of Hedgehogs and Gli2 in zebrafish muscle development using two mutant strains; sonic-you (syu) and you-too (yot), respective for sonic hedgehog (shh) and Gli2 mutation [5].

Anatomical context of gli2a

• Motor neuron induction at all axial levels was reduced in yot (gli2(DR)) mutant embryos [3].
• In flh, syu, and yot mutants, glomeruli differentiate at ectopic lateral positions within the embryo and contain morphologically identifiable podocyte and endothelial cell types [6].
• We show here that the zebrafish midline mutants you-too (yot) and iguana (igu) develop lenses from the adenohypophysis anlage [4].
• In yot mutant embryos, development of slow muscles was completely blocked, whereas in syu mutant embryos, a small number of slow muscle cells could still form, suggesting that other Hhs were also involved in slow muscle induction [5].
• We show that the absence of myotomal adaxial cells in you-too/gli2 embryos severely impairs secondary motor axonal pathfinding, including their ability to project into the somites [7].

Regulatory relationships of gli2a

• Induction of slow muscles by other Hhs appeared to require Gli2, because ectopic expression of Echidna hedgehog (Ehh) and Tiggy-winkle hedgehog (Twhh) failed to induce slow muscles in yot mutant embryos [5].
• Minhas et al. 2015 have elucidated a subset of cis-regulatory elements controlling GLI2 expression. They have shown that conserved non-coding elements (CNEs) from the intron of GLI2 gene act as tissue-specific enhancers and reporter gene expression induced by these elements correlates with previously reported endogenous gli2 expression in zebrafish. The regulatory activities of these elements are observed in several embryonic domains, including neural tube and pectoral fin [Ref].

Other interactions of gli2a

• Zebrafish wnt4b expression in the floor plate is altered in sonic hedgehog and gli-2 mutants [8].

References