Deletion of sequence from -877 to +1266bp relative to the nau transcription start site.
Deletion reported as extending from -877 to +1266 relative to the nau transcription start site. This corresponds to a region of 2112bp on the reference sequence. The deletion coordinates were determined from junction sequences in Figure 2.
nau188 embryos exhibit randomisation of the DA3 attachment sites between the wild type DA3 and DO5 positions, as well as the formation of unstructured fibres not resembling any particular muscle. Even when correctly orientated, mutant DA3 fibres are generally thinner than wild type, despite a normal or slightly reduced number of nuclei per cell. In addition, there are many cases of either loss or mis-formation of the DA3, DO4 and DO3 muscles, while other muscles are hardly affected. The severity of these phenotypes vary from embryo to embryo and between segments within the same embryo. There are a small number of DA3>DA2 transformations.
In homozygous nau188 mutant embryos the DA3 muscle is completely absent in around 5% of segments, abnormal in orientation in 45% and normal looking in about 50% of segments. The DA3 fibres in the normal looking nau188 muscles contain only seven nuclei on average compared to approximately 9 in wild type.
Homozygous embryos show a range of muscle defects.
Approximately 50% of homozygous embryos do not survive to the pupal stage
Homozygous embryos have a somatic muscle phenotype, in which only a small subset of somatic muscles is affected, including muscles DO4 and DA3. 39% of homozygous eggs derived from homozygous female germline clones (lacking both maternal and zygotic nau function) survive to adulthood. The remaining 61% of eggs appear to be unfertilised. Homozygous embryos derived from homozygous female germline clones show somatic muscle defects identical to those seen for nau188 zygotic mutants, with the most severely affected muscles including DO4 and DA3.
nau188 has muscle cell of A1-7 dorsal acute muscle 3 phenotype, enhanceable by kn[+]/kncol85-GAL4
nau188 has muscle cell of A1-7 dorsal acute muscle 3 phenotype, enhanceable by kncol85-GAL4/kncol85-GAL4
kn[+]/kncol85-GAL4, nau188 has muscle cell of A1-7 dorsal acute muscle 3 phenotype, suppressible by knUAS.Tag:HA/Scer\GAL4kn-col85-GAL4
kncol85-GAL4/+ and, more so, kncol85-GAL4/kncol85-GAL4 aggravates the DA3 muscle defects seen in nau188 embryos. Inclusion of kncol85-GAL4 also increases the number of ill-formed muscles at the expense of DA3>DA2 muscle transformations. However, the fraction of DA3>DO5 transformations and DA3 +DO5 bifid fibres is not significantly increased by lowering kn levels.
Scer\GAL4kn-col85-GAL4-mediated expression of knScer\UAS.T:Ivir\HA1 fully rescues the DA3>DA2 phenotype and decreased the number of ill-formed muscles of nau188, kncol85-GAL4/+ animals. The fraction of DA3>DO5 transformations and bifid fibres is unaffected.