The ectodomain of Tmem2 is critical for proper AVC differentiation. In situ hybridization indicates expression of bmp4 in wild‐type (A, C, E, G) embryos and Ztmem2 (B, D, F, H) mutant siblings at 48 hours post fertilization (hpf); frontal views. In wild‐type (wt) embryos, concentrated expression of bmp4 is restricted to the AVC (A, arrowheads), whereas bmp4 is broadly expressed throughout the ventricle in Ztmem2 mutants (B, bracket). Expression of full‐length tmem2 can restore the enriched concentration of bmp4 expression in the AVC of Ztmem2 mutants (D, arrowheads; Table 1); additionally, expression of full‐length tmem2 does not affect bmp4 expression in wt siblings (C, arrowheads; Table 1). Expression of full‐length tmem2 also improves cardiac looping and AVC constriction in Ztmem2 mutants (D). Similarly, expression of htrc‐tmem2 can rescue the bmp4 expression pattern in Ztmem2 mutants (F, arrowheads; Table 1), but does not disrupt bmp4 expression in wt siblings (E; Table 1). Finally, as with ΔC‐term and all other extracellular domain deletion variants, expression of the ΔG8 variant provides no evident rescue of the bmp4 expression pattern in Ztmem2 mutants (H, bracket; Table 1) and does not affect bmp4 expression in wt embryos (G, arrowheads; Table 1)
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