IMAGE

Fig. 3

ID
ZDB-IMAGE-110624-41
Genes
Source
Figures for Putiri et al., 2011
Image
Figure Caption

Fig. 3

Induction of endoderm-specific genes is affected in maternally mutant mis embryos. Analysis of germ layer gene markers in wild-type (A,C,E,G,I,K,M) and maternally mutant mis embryos (B,D,F,H,J,L,N). Ectodermal markers chordin (A,B) and foxb1.2 (C,D) are induced in wild-type and mis mutants at similar levels, although their anterior-most domains of expression (arrows in A,C) are absent in mis mutants. Mesodermal marker genes no tail (E,F), snail1a (G,H), and lhx1a (I,J) are also induced in the blastoderm margin at normal levels in mis mutants compared to wild-type. On the other hand, mis mutant embryos fail to activate endodermal markers foxA2 (K,L) and sox17 (M,N) in the “salt and pepper” pattern characteristic of endodermal cells (brackets in K,M, compare to no detectable expression in L,N). The axial mesodermal domain of foxA2 (arrowheads in K,L) does become induced in mutant embryos, albeit in an abnormally shaped domain likely caused by the morphogenesis defects associated with the mutation (a similar effect is observed with regards to the axial domain of zlim-1 arrowhead in (I); see also Supp. Fig. 2). Expression of sox17 in forerunner cells (arrowhead in M) is absent in the mutant (N) (see text). Stages are 5 h.p.f. (E,F), 6 h.p.f. (G–J,M,N), and 8 h.p.f. (A–D,K,L). All images are dorsal views with the animal pole at the top, except (E,F) which are animal views.

Figure Data
Acknowledgments
This image is the copyrighted work of the attributed author or publisher, and ZFIN has permission only to display this image to its users. Additional permissions should be obtained from the applicable author or publisher of the image.

Reprinted from Developmental Biology, 353(2), Putiri, E., and Pelegri, F., The zebrafish maternal-effect gene mission impossible encodes the DEAH-box helicase Dhx16 and is essential for the expression of downstream endodermal genes, 275-289, Copyright (2011) with permission from Elsevier. Full text @ Dev. Biol.