Ectopic expression of vgScer\UAS.T:Ivir\HA1 within the lateral transverse (LT)1-4 muscles (under the control of Scer\GAL4Mef2.PR) causes them to migrate toward the segment borders and attach there, producing muscle-muscle attachments between LT and VA muscles, where they normally do not occur. This ectopic expression does not seem to alter the initial muscle identities of LT2, LT4, and ventral acute muscle 2. The ectopic muscle-muscle adhesions induced by ectopic expression of vgScer\UAS.T:Ivir\HA1 in the LT muscles seems to be functional, because muscle VA1 is often located away from its normal position due to tension produced by abnormal attachment to the LT muscles.
Expression of vgScer\UAS.T:Ivir\HA1 under the control of Scer\GAL4Mef2.PR does not affect the formation of the midgut constrictions in the embryo.
Expression of vgScer\UAS.T:Ivir\HA1 under the control of Scer\GAL4Mef2.PR results in the loss of muscles VO4-VO6, although the overall organisation of the remaining muscles appears normal.
Expression of vgScer\UAS.T:Ivir\HA1 under the control of Scer\GAL4Mef2.PR does not affect the Mef2-positive cardiac cells, but causes two additional tin-positive cardiac cells per hemisegment.
Scer\GAL4Mef2.PR, vgUAS.Tag:HA has muscle attachment site | ectopic phenotype, suppressible by sdΔ88-159.UAS/Scer\GAL4Mef2.PR
Scer\GAL4Mef2.PR/vgUAS.Tag:HA is an enhancer of muscle attachment site | ectopic phenotype of sli2
The muscle detachment phenotype found in vgnull; rhea1 double mutant embryos appears to be solely due to a lack of vg activity as it can be rescued through expression of vgScer\UAS.T:Ivir\HA1 in muscle cells.
Co-expression of both vgScer\UAS.T:Ivir\HA1 and sdΔ88-159.Scer\UAS in developing muscles under the control of Scer\GAL4Mef2.PR results in fewer ectopic muscle attachments (24.5% compared with 81.8% when vgScer\UAS.T:Ivir\HA1 is expressed alone).
Embryos co-expressing vgScer\UAS.T:Ivir\HA1 and sdScer\UAS.T:Zzzz\FLAG under the control of Scer\GAL4Mef2.PR show complete disruption of the organisation of muscle fibres and muscle cell attachment.
Co-expression of vgScer\UAS.T:Ivir\HA1 and Mef2Scer\UAS.T:Hsap\MYC under the control of Scer\GAL4Mef2.PR in the embryo has a synergistic effect on cardiac cells; there are two extra rows of Mef2-positive cardiac cells and six tin-positive cardiac cells per hemisegment, with many more tin-positive pericardial cells.
Co-expression of sdScer\UAS.T:Zzzz\FLAG and vgScer\UAS.T:Ivir\HA1 under the control of Scer\GAL4Mef2.PR in the embryo results in the loss of almost all Mef2-positive cardiac cells and dislocation of all tin-positive cells into the somatic muscle region.