wing & macrochaeta
Homozygous loss of salm in the muscle (generated by inducing the Df(2L)salmFRT deletion in muscle using UAS-FLP under the control of Scer\GAL4Mef2.PR, in trans to salm1) results in complete tubular reversion of the indirect flight muscles.
Dorsal trunk cells are transformed into visceral branch identity in salm1 embryos. The tips of the transformed branches contain terminal cells and fusion cells, as in the lateral trunk of wild-type embryos.
Single cell class IV dendrite arborisation (da) neuron clones that are homozygous for salm1 do not show defects in the establishment or maintenance of dendritic tiling.
Extra lateral chordotonal organs are formed in mutant embryos, with the number of lateral chordotonal organs in the cluster frequently being 6 or 7 (instead of the wild type 5). The extra chordotonal organs are restricted to the lateral cluster with the other abdominal chordotonal organs (V'ch1, VchAB) remaining wild-type in number.
Clone on the dorsal surface of the wing between wing vein L2 and L3 causes branching of the wing vein L2 on the presumptive dorsal surface; forked L2 phenotype. The ectopic vein forms within and at the extreme anterior edge of the clone. When the clone extends to the margin ectopic triple row bristles are formed. Clones near the posterior wing edge cause bifurcation of wing vein L5 or the posterior crossvein.
Defects in the identity of posterior segments A8 and A9, distinct posterior spiracles are not formed.
Anterior prothoracic pattern elements differentiate in the labial segment, two abdomen segments are replaced with thoracic segments.
embryonic lethal. Shows partial homeotic transformation of labium to prothorax and of A9 and 10 toward A8. Point mutants judged to be amorphic or nearly so judging from the phenotype of salm/Df compared with salm/salm. salm; Abd-B double mutants exhibit thoracic structures in parasegments 14 and 15; similarly, salm and Scr seem to act independently on head structures in parasegments 2 and possibly 1.
salm1 has lethal | embryonic stage phenotype, suppressible by salaC20-sal
salm1 has wing vein L2 | ectopic phenotype, suppressible by kniri-1
salm1 has dorsal row of triple row of wing sensilla | ectopic phenotype, non-suppressible by kniri-1
salm1 has medial row of triple row of wing sensilla | ectopic phenotype, non-suppressible by kniri-1
salm1 has ventral row of triple row of wing sensilla | ectopic phenotype, non-suppressible by kniri-1
salm1, tkv4 has tracheal section phenotype
Embryos doubly mutant for rib1 and tkv4 form only the transverse connectives and visceral branches. The addition of salmScer\UAS.cKa and Scer\GAL4btl.PS to rib1 embryos does not rescue the dorsal trunk migration phenotype.
Embryonic lethality and the homeotic effects can be rescued by the salaC20-sal construct, individuals die as crawling larvae.