UASt regulatory sequences drive expression of a 500bp inverted repeat.
Expression of PaxNIG.18061R under the control of Scer\GAL4Vm26Aa.F results in moderate dorsal appendage defects in 15% of cases and strong defects in 6% of cases, with the appendages being rough.
Expression of PaxNIG.18061R under the control of Scer\GAL4CY2 results in moderate dorsal appendage defects in 48% of cases, with the appendages being short.
Compared with wild-type, an increased number of unfused myoblasts are detected in embryos expressing PaxNIG.18061R under the control of Scer\GAL4how-24B.
Expression of PaxNIG.18061R under the control of Scer\GAL4how-24B causes loss of nuclei from muscles VA2 and DT1, and no change in DA1, SBM, or VT1 muscles.
Expression of PaxNIG.18061R under the control of Scer\GAL4how-24B leads to a reduced rate of embryonic myoblast fusion (relative to wild-type) measured in VA2.
PaxNIG.18061R, Scer\GAL4Vm26Aa.F has dorsal appendage phenotype, enhanceable by ttk[+]/ttktwp
PaxNIG.18061R, Scer\GAL4CY2 has dorsal appendage phenotype, enhanceable by ttk[+]/ttktwp
PaxNIG.18061R, Scer\GAL4how-24B has dorsal transverse muscle cell phenotype, enhanceable by Mp20NIG.4696R, Scer\GAL4how-24B
PaxNIG.18061R, Scer\GAL4how-24B has muscle cell of ventral acute muscle 2 phenotype, enhanceable by Mp20NIG.4696R, Scer\GAL4how-24B
PaxNIG.18061R, Scer\GAL4how-24B has nucleus phenotype, enhanceable by Mp20NIG.4696R, Scer\GAL4how-24B
The severity of the dorsal appendage defects caused by expression of PaxNIG.18061R under the control of either Scer\GAL4Vm26Aa.F or Scer\GAL4CY2 is enhanced by ttktwp/+.
Co-expression of Mp20NIG.4696R and PaxNIG.18061R under the control of Scer\GAL4how-24B induces a strong decrease in the number of DT1 and VA2 nuclei, two muscles affected by single RNAi knockdowns. In contrast, the phenotype of single knockdowns in SBM is not enhanced by the double knockdowns.