Fig. 3. Loss of maternal Gug activity affects embryonic segmentation and Tsh expression. (A) Ventral view of a wild-type larva showing the 11 similar trunk segments each with alternating denticled and naked cuticle. (B) Detail of the head region of an embryo homozygous for Gug³⁵. (C-E) Larvae from Gug³⁵ germline clones fertilised by wild-type (C) or Gug³⁵ (D,E) sperm. (C) Note the reduced number of segments compared with wild type. (D) Note the holes in the cuticle or the absence of the ventral cuticle (E). (F) Phenocopy of the Gug segmentation phenotype after injection of antisense Gug mRNA into embryos (compare with C). Expression of the segmentation genes ftz (G), hb (H), Kr (I), kni (J) and the region-specific homeotic protein Tsh (K) in wild type (left) and Gug mutant (right) embryos. Gug/Gug zygotes were distinguished by the absence of ftzlacZ (carried on the TM3 balancer chromosome) expression. Loss of Gug generally increases the number of cells expressing the segmentation genes. Note that Tsh is missing from the ventral parts (arrow) and in stripes in dorsal regions (arrowheads) of the trunk in Gug^– embryos (K, right panel), where Tsh is uniformly expressed in the trunk of wild-type embryos (K, left panel).