Genomic deletion that begins in the first coding exon of Tm2 and extends past the final coding exon.
A subset of Tm2Δ8-261/Df(3R)BSC741 embryos display some defects in myotube elongation in lateral transverse muscles 1-3 and lateral longitudinal muscle 1; but do not display any significant difference in the size of the dorsal oblique muscle 2 as compared to controls.
Tm2Δ8-261 has some die during embryonic stage | recessive phenotype, suppressible | partially by Scer\GAL4Mef2.PU/Hsap\TPM2UAS.GFP
Tm2Δ8-261 has increased mortality during development | recessive phenotype, suppressible | partially by Scer\GAL4Mef2.PU/Hsap\TPM2UAS.GFP
Tm2Δ8-261 has some die during embryonic stage | recessive phenotype, suppressible | partially by Scer\GAL4Mef2.PU/Hsap\TPM2K49Del.UAS.GFP
Tm2Δ8-261 has increased mortality during development | recessive phenotype, suppressible | partially by Scer\GAL4Mef2.PU/Hsap\TPM2K49Del.UAS.GFP
Tm2Δ8-261 is partially rescued by Tm2K49Del.UAS.GFP/Scer\GAL4Mef2.PU
Tm2Δ8-261 is partially rescued by Scer\GAL4Mef2.PU/Tm2UAS.GFP
Df(3R)BSC741/Tm2Δ8-261 is partially rescued by Scer\GAL4kirre-rP298-G4/Tm2cDNA.UAS.EGFP
Expression of Tm2cDNA.Scer\UAS.T:Avic\GFP-EGFP under the control of Scer\GAL4kirre-rP298 leads to partial rescue of the myotube elongation defects of Tm2Δ8-261/Df(3R)BSC741 mutant embryos, but does not lead to any significant difference in the size of the dorsal oblique muscle 2 as compared to controls.