Fig. 6
- ID
- ZDB-FIG-121204-16
- Publication
- Yabe et al., 2012 - Mesogenin causes embryonic mesoderm progenitors to differentiate during development of zebrafish tail somites
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Msgn1 functions as a transcriptional activator in tail PSM formation. (A) Schematic representation of msgn1 mutants. ΔN-Msgn1 lacks most of the N-terminal region, and the Δbasic form of Msgn1 lacks only the basic domain. In VP16-Msgn1 and EnR-Msgn1, the transcriptional activator domain of VP16 and the transcriptional repressor domain of Engrailed of Drosophila melanogaster, respectively, were fused to the N-terminus of the ΔN-Msgn1. These mutant forms were connected to the C-terminal region of the mCherry with the 2a peptide, designed to be expressed under the control of the msgn1 promoter, and injected into spt mutant eggs by using the tol2-based micro-injection system with msgn1 MO. (B)-(E) The ΔN-msgn1 was able to rescue the tbx24 expression in the PSM (B, n=33,100%), whereas the Δbasic form was not (C, n=24,100%). The tbx24 expression in msgn1-injected spt mutant embryos was rescued by the VP16- (D, n=28,100%) but not by the EnR- (E,n=29,100%) Msgn1. |
Reprinted from Developmental Biology, 370(2), Yabe, T., and Takada, S., Mesogenin causes embryonic mesoderm progenitors to differentiate during development of zebrafish tail somites, 213-222, Copyright (2012) with permission from Elsevier. Full text @ Dev. Biol.