Fig. 7. nos– mutants have a milder effect (A) Internally controlled bcd PAT assay from wild type (lanes 1-9) and nos– (lanes 1'-9') RNAs from ovaries (lane 1,1') or embryos (lanes 2-9,2'-9', 25°C). C1, 
bcd cDNA control; C2, osk PCR control (no template). While nos– mutants exhibit some delayed bcd deadenylation (compare lane 8' with lane 8), the bcd polyA tail profile returns to a wild-type one in the final time point (lane 9' versus lane 9). By contrast, pum– embryos show a stronger deadenylation defect in the equivalent time course (compare the ratio lane 9:lane 9' here with lane 9:lane 9' in Fig. 2B). Note, each mutant set can only be compared with its parallel wild-type collection. (B) Western blot of wild-type (lanes 2-9) and nos– (lanes 2'-9') extracts probed for Bicoid (time course as in A). A nonspecific crossreactive band of slightly lower mobility than Bicoid appears in nos– extracts. (C) Scanning electron micrograph of nos– heads (frontal view). Four percent of nos– cuticles exhibit a protrusion analogous to pum– (severe), 29% showed a smaller variably sized protrusion (moderate) and 67% had no such abnormality (unaffected). n=52. Scale bar: 20 µm.
