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. 2008 Sep 19;3(9):e3241. doi: 10.1371/journal.pone.0003241

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Grieder et al.

This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are properly credited.

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Live imaging of embryonic tracheal development in mutant and rescued embryos. Tracheal development was followed in live embryos using an αCat-GFP transgene specifically expressed in the tracheal system under the control of btl-Gal4. Pictures of late stage embryos were taken from movies (see supporting material) of the following genetic makeup: (A) btl-Gal4 UAS-αCat-GFP; γCOP¹⁰/γCOP¹⁰. (B) btl-Gal4 UAS-αCat-GFP; Ω35-17 sr¹ e^s γCOP¹⁰/ Ω35-17 sr¹ e^s γCOP¹⁰. (C) btl-Gal4 UAS-αCat-GFP/UASp-γCOP; γCOP¹⁰/γCOP¹⁰. (D) btl-Gal4 UAS-αCat-GFP; UAS-pio γCOP¹⁰/γCOP¹⁰. Strikingly, the dorsal branches are frequently disrupted in γCOP¹⁰ mutants (see arrows in A and Movie S1), similar to the phenotype observed in pio and dp mutants [8]. Dorsal trunk fusion defects are also observed in mutants (arrowhead in A). Both defects were rescued either by expressing a genomic γCOP rescue transgene (B), or by expressing γCOP specifically in the tracheal system using the UAS/Gal4 system (C). Tracheal-specific expression of Pio protein rescues the dorsal branch defects; however, dorsal trunk fusion defects are still visible (arrowhead in D).