Fig. 4. Failure of direct repression of E(spl)m8 by Su(H) can extinguish the SOP cell fate. (A) Part of notum region of an adult fly carrying two copies of an E(spl)m8 genomic DNA transgene (see Fig. 2A, construct 1), showing a normal pattern of adult mechanosensory bristles. Labeled macrochaetes: ASA, anterior supraalar; PSA, posterior supraalar; APA, anterior postalar. (B) Same region from a fly carrying two copies of the E(spl)m8 Sm transgene [Su(H) binding sites mutated], showing loss of the PSA bristle (broken circle). (C,C',D,D') The cellular basis of bristle loss caused by the E(spl)m8 Sm transgene is failure of SOP specification. (C,C') Same genotype as A; (D,D') same genotype as B. (C,D) Late third-instar wing discs stained with anti-Sens antibody to mark SOPs. (C',D') Higher-magnification views of the regions boxed in C and D, respectively. Labeled SOPs: PNP, posterior notopleural macrochaete; ANWP, campaniform sensilla of the anterior notal wing process. Broken circle in D' indicates position of missing PSA SOP. The presence of both ANWP SOPs indicates that both discs are at a stage late enough to observe the PSA SOP in wild-type discs. (E) Frequency of bristle loss is significantly greater in E(spl)m8 Sm homozygous flies (red) than in flies homozygous for the wild-type E(spl)m8 transgene (blue). Mann-Whitney U test: U=2, P=0.002.