Fig. 3. Embryonic loss-of-function phenotypes of mib2 alleles. (A-C) Lateral views of the ventral region of stage 16 wild-type (A), mib2¹ (B) and mib2¹ (C) germline clone Drosophila embryos stained with anti-myosin (A,B) or anti-Tropomyosin (C). Positions of VA2, VT1 and VO muscles are indicated. Note the presence of unfused myoblasts (black arrowheads in B,C), the absence of muscles in the VL region (asterisks in B,C, and muscle scheme in Fig. 4G), and presence of myospheres (arrow, B). Whole-embryo pictures (below) are focused on the gut. White arrowheads point to the position of the first midgut constriction (A) and to the unfolded midgut (B,C). (D,E) Dorsal views focused on the DA1 muscle of mib2¹/CyO and mib2¹ stage 15 embryos, respectively. Arrowheads point to Eve-labelled nuclei (green). Asterisks mark nuclei of pericardial cells. (F) Number of eve-expressing nuclei in DA1 muscles of embryos of the indicated genotype (n, number of hemisegments quantified). (G-J) Progressive degeneration of muscles in mib2¹ embryos. Muscles were revealed by Mhc--GFP (G,I,J) and by anti-Tm staining (H). At stage 15 (H), all muscles are present and attached to the apodemes (arrowhead, unfused myoblast). At stage 16 (I), some muscle attachments are becoming thinner (arrowhead), while others, many in the VL region, have detached (arrows). In L1 larvae, most muscles are missing (J). (K) Scheme indicating percentages of specific muscles that remain attached to apodemes in mib2¹ first instar larvae: red (80-100%), blue (50-80%), yellow (10-25%) and white (<10%) (n=50 abdominal hemisegments; 2 to 5 examined).