As a result of a PCR artifact and an error in notation, the deletion in the Prm1 allele was stated to be 4kb in size in FBrf0159031. Reanalysis of the data, as well as additional cloning and sequencing indicate that the deletion is actually 1.05kb in length and is internal to the P-element. The deleted region encompasses portions of the upstream region and first exon of the w gene, removing 163 codons.
FlyBase curator comment: FBrf0159031 states that the lesion in Prm1 is the deletion of a 4kb fragment 5' to the second nucleotide of the transcription start site. However, this is in error - see FBrf0184062 for subsequent revision of this data.
The authors retract the statement in FBrf0159031 that Prm1 homozygotes exhibit a myoblast fusion phenotype. Experiments subsequent to publication now indicate that this phenotype may be due to a TM3 balancer that was mis-indentified.
The banding patterns of myosin and actin in Prm1 homozygous mutant embryo wall muscles is completely disrupted. In wild-type, well-organised sarcomeres are formed in somatic muscle fibers. Sarcomeres are severely disrupted in Prm1 mutant embryos, Z-bodies are poorly organised, the length of myofilaments are greatly reduced and bundles of myofilaments associated with these Z-bodies are not parallel. Prm1 homozygous mutant embryos have reduced thick filament numbers. However, thin filament number in the same area is relatively unaffected. This leads to some areas of myofibrils completely lacking thick filaments. Compared to wild-type, thick filaments of Prm1 embryo body wall muscles are solid. Dense particles in the periphery collapse into the center, forming filled thick filaments. The diameters of thick filaments are also not even.
Prm1 is rescued by PrmS-A3.cLa
Prm1 is rescued by PrmS18A.cLa
Prm1 is rescued by PrmS-A4.cLa
Prm1 is rescued by PrmS10A.cLa
The transgenes PrmS10A.cLa, PrmS18A.cLa, PrmS-A3.cLa, and PrmS-A4.cLa rescue the embryonic lethal phenotype of Prm1 to adulthood.