High impact information on eng2a

• We also show that, consistent with results obtained using other methods, uncaging eng2a (which encodes the transcription factor Engrailed2a) in the head region during early development causes a severe reduction in the size of the eye and enhanced development of the midbrain and the midbrain-hindbrain boundary at the expense of the forebrain [1].
• In situ hybridizations demonstrate that antibody injection causes downregulation of pax[b] transcripts in the posterior midbrain and alteration of wnt-1 and eng-2 expression in this area [2].
• Thus, Eng2/Eng3 and Fgf8 are necessary to maintain midbrain identity in the neural plate and thereby position the DMB [3].
• Transplantations, mRNA injections and morpholino knock-down experiments show that this feedback regulation of pax2.1 transcription occurs cell-autonomously, and that it requires eng2 and eng3 as known targets for Pax2.1 regulation [4].
• The relative organization of ache, eng2, and shh genes is conserved between zebrafish and mammals and defines a synteny [5].

Biological context of eng2a

• Consistent with this model, we demonstrate that zebrafish Engrailed and Pbx interact in vitro and that this interaction is required for both the eng2a overexpression phenotype and Engrailed's role in patterning the MHB [6].

Anatomical context of eng2a

• A second site of activity was observed in each somite where specific myotomal cells, the muscle pioneers, express eng-2 [7].
• In the hindbrain, eng-2 expression seems restricted to the primordium of the cerebellum [7].
• The data are consistent with there being a temporal and spatial requirement for Hsp90 function within somitic cells which is necessary for the formation of eng-2-expressing muscle pioneers and possibly other striated muscle fiber types [8].

Associations of eng2a with chemical compounds

• Within the somites, geldanamycin treatment results in the absence of eng-2-expressing muscle pioneer cells [8].

Other interactions of eng2a

• We find that Fgf8 is a candidate for this signal, as it is both necessary and sufficient to repress pax6.1 and hence to shift the DMB anteriorly independently of the expression status of eng2/eng3 [3].

Analytical, diagnostic and therapeutic context of eng2a

• The embryonic expression of the eng-2 gene was analysed by in situ hybridization to whole-mount embryos and tissue sections [7].

References