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We found that in dpn and dpn Def1D6 clone cells that cross the d/v boundary, the expression of Wg was slightly but consistently reduced, while the expression of Cut was not affected.
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Unexpectedly, we found few targets in the head for either pathway, although these domains correspond to the vertebrate midbrain-hindbrain boundary and the expression of several highly conserved Tribolium head patterning genes is initiated there (Posnien et al., 2011).
By contrast, marking cell boundaries by the expression of GFP-CAAX (Fig. 2B B″), or co-staining with ZO1 (Fig. 2C) showed equal fluorescence intensity for all cell borders.
The Anteriormost incorporated segment (trunk segment 15) shows traces of a segment boundary, mostly adaxially: the expression of the boundary is weaker, however, than the fully-expressed boundaries of the free trunk segments.
This boundary condition is the expression of the mass balance on the boundary, which is obtained by using the standard Cauchy tetrahedron argument.
In the latter case, the genes that define the juvenile boundary may repress the expression of adult leaf-promoting genes above a certain threshold.
In wild type wing discs, activation of the Notch pathway at the dorsal-ventral boundary leads to the expression of target gene products, such as the signaling molecule Wingless (Wg) [ 49].
Conversely, in the more posterior areas, hairy1 transcripts are present ventrally in the midbrain but are absent from the mid- and hindbrain boundary, contrary to the expression of Hes1 in the mouse and the hairy-related genes her5/9 in zebrafish.
Finally, forced expression of Cut in non-boundary cells represses the expression of Wg target genes (Figure 4D and Figure S1).
In cut6 mutant discs, the early activation of Notch at the DV boundary, as shown by the expression of Wg, is comparable to wild-type discs (compare Figures 6B and 6D).
Imprinted gene cluster DMRs may act as boundary elements and/or regulate the expression of imprinted non-coding RNAs (for example, H19, KCN1OT and Air) and the methylation status of the DMR is critical to their normal function.
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