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. Author manuscript; available in PMC: 2014 May 1.
Published in final edited form as: Dev Biol. 2013 Mar 14;377(1):10.1016/j.ydbio.2013.02.020. doi: 10.1016/j.ydbio.2013.02.020

Fig. 3.

Fig. 3

Salivary gland migration defects in Rac mutant embryos. Salivary glands of rac1J11rac2Δ mutant embryos (B), embryos expressing Rac1N17 in the gland at high levels (C) and embryos expressing Rac1N17 in the gland at moderate levels (D) initiate posterior migration by turning at the distal tip (B–D, arrows) although the proximal cells have not migrated dorsally (B–D, arrowheads) at stage 12. In stage 13 and 14 (J–L) salivary glands of rac1J11rac2Δ mutant embryos (F and J), embryos expressing Rac1N17 in the gland at high levels (G and K) and embryos expressing Rac1N17 in the gland at moderate levels (H and L), the distal tip does not continue migrating posteriorly (F–H and J–L, arrows) and the proximal cells do not migrate dorsally (F–H and J–L, arrowheads). Graph shows percentage of salivary glands that turn completely, turns halfway, turns only at the distal tip or does not turn in rac1J11rac2Δ mutant embryos, embryos expressing Rac1N17 in the gland and rescue embryos (M). All embryos shown were stained for dCREB with embryos in B, F and J being additionally stained for β-gal to distinguish heterozygous from homozygous siblings (not shown). Scale bar represents 20 μm.