Figure 3

Alary muscle attachment defects caused by EMS-induced mutations in the collagen IV-encoding gene Cg25C . (A-I) Live preparations of Cg25C mutant embryos with GFP and RFP markers as in the corresponding control in Figure 1A and raised at 25°C. The embryo in panel B additionally carries Mhc-tau::GFP as the corresponding control in Figure 1D. (A) Homozygous Cg25C^S3064 embryo at early stage 17 in which some alary muscles (AMs, arrows) start to detach from the dorsal vessel. The LVM is normal. (B) The body wall musculature develops mostly normally in homozygous Cg25C^S3064 mutants. (C) Hemizygous Cg25C^S3064 embryo with the Cg25C-deleting deficiency Df(2L)Exel7022 at early stage 17 as (A), but with AMs still attached to the dorsal vessel. (D) Cg25C^S3064/Df(2L)Exel7022 embryo at late stage 17, in which many AMs, particularly in the middle portion, lose their dorsal vessel attachment. (E) Late stage 17 embryo homozygous for Df(2L)Exel7022, in which both collagen IV-genes, Cg25C and vkg, are deleted, shows no enhancement in the detachment phenotype as compared to Cg25C^S3064 homo- and hemizygotes. (F) AM detachment is also apparent in the majority of stage 17 embryos of the genotype Cg25C^DTS-L3/Cg25C^S3064. A milder detachment phenotype is observed in a fraction of late stage 17 embryos for the alleles Cg25C^S0791(G) and Cg25C^S1348(H). (I) Alary muscle detachment also occurs in the combination Cg25C^S0120/Cg25C^S3064. (J) Schematic of Cg25C-encoded collagen IV illustrating the positions of the mutations found in the indicated EMS alleles. The collagen triple helix-forming domain (red) consists of Gly-X-Y repeats that are interrupted at positions marked by vertical bars. All mutations found in this study are missense mutations at the glycine of a Gly-X-Y repeat (underlined in the sequence with flanking repeats shown to the right).