Figure 1.
The outstretched wing phenotype.
(A) Wild type (w1118) adult male Drosophila melanogaster showing typical resting wing posture. (B) Adult males hemizygous for the oso allele showing their typical resting wing posture. (C–F) Adult males of the indicated hemizygous genotypes showing resting wing postures typically associated with the outstretched phenotype. Dorsal (C,D) and ventral (E–F) views are shown. The angle of the wing relative to the body axis (dotted lines) is indicated. (G–J) Eyes of the indicated genotypes. Extent of ventral eye field is outlined by dashed line. Minor ventral eye size reduction (arrows) is visible in oss and os1 alleles.
Figure 2.
Structure of the os1 hinge and adult musculature.
Scanning electron micrographs of the adult dorsal (A–D) and ventral (E–F) wing hinge regions of wild type (A, E) and os1 (B–D and F) individuals. The relative expressivity of the os1 allele phenotypes is indicated by ‘weak’ ‘moderate’ and ‘strong’ labels. Note how increasing phenotypic strength is associated with the progressive loss of the AS1, AS2 and PNWP. Wing hinge structures are named in [25]. Unnamed plate (UP), first, second and third auxiliary sclerites (AS1, AS2 and AS3), anterior notal wing process (ANWP) and posterior notal wing process (PNWP) are present in the dorsal hinge. In the ventral hinge, auxillary pouch (AP) and proximal ventral radius (PVR) are shown. (G–J) Longitudinal sections through adult males of the indicated genotypes show the structure of the primary flight muscles.
Figure 3.
Expression of upd and activation of JAK/STAT pathway signalling in the wing disc.
Proximal (P), medial (M) and distal (D) folds are labelled. Scale bar is 100 µm, (A & B) Third instar wing imaginal discs showing the expression of upd mRNA in wild type (A) and oso (B) individuals. Expression of upd within the P fold (arrow) is lost in the oso mutant. (C & D) Third instar wing imaginal discs showing DNA (white) and the 10xSTATGFP reporter (green) in wild type (C) and oso (D) individuals. Reporter activity within the P fold (arrow) is greatly reduced in oso mutants suggesting that JAK/STAT pathway ligands are not expressed in this area. (E) Schematic representation of the third instar wing imaginal disc fate map showing the regions labelled in Figure 2, the P, M and D lateral folds and the approximate regions of wild type upd expression (purple). Image based on fate map originally published in [25].
Figure 4.
JAK/STAT signalling and fold formation.
Proximal (P), medial (M) and distal (D) folds are labelled. (A) Wild type third instar wing imaginal discs showing the pattern of 10xSTATGFP reporter activity (green), FasIII (red) and DNA (blue). The approximate position of the XZ sections shown in B–E is indicated by the dotted line. (B) An XZ section through the lateral wing folds of wild type third instar wing imaginal disc showing F-actin (red in B and white in B’) and the 10xSTATGFP reporter (green in B and white in B”). (C–E) XZ sections through third instar wing imaginal discs of males hemizygous for the oso allele stained to visualise F-actin (white), and hence disc structure. The P fold is reduced in depth in C and D (arrows) and is missing completely in E.
Figure 5.
Modulation of JAK/STAT activity phenocopies os defects.
(A) Dorsal hinge region of a third instar wing imaginal disc from a 10xSTATGFP, ptc>Gal4/UAS-stat92E RNAi individual showing the extent of 10xSTATGFP reporter activity (green in A, white in A’) and FasciclinIII (red in A, white in A”) to outline cell shape. P, M and D folds are labeled and the domain in which reporter activity is ablated following knockdown of stat92E is shown (arrow in A’), (B–C) Adult male flies of the indicated genotypes showing resting wing posture. Knockdown of stat92E mRNA in the ptc domain produces a clear and highly penetrant wings held out defect. (D) SEM of the dorsal wing hinge of a ptc>stat92E RNAi male with a wings held out phenotype. Compared to a wild type hinge (Figure 2A) both the first and second auxiliary sclerites (AS1 and AS2) are reduced.