zfh15 and zfh15/zfh175.26 embryos show defects in the formation of ventral motor nerves. The ISN nerve is always present in these mutants but has branching defects. This nerve exits the CNS, but the ISNb and SNa nerves are truncated or absent. The SNc and ISNd nerves are not identifiable in these mutant embryos and it may be that the CNS stops developing before the formation of these minor nerves.
Normal denticle belts but abnormal mouthhooks. Mesoderm phenotypes similar to zfh12. Somatic musculature shows variable patterning and insertion site positioning defects, principally in the ventral oblique and the dorsal muscles. These pattern defects are evident at the segregation of the muscle precursors, as revealed by an aberrant pattern of S59 gene expression. Midgut development is abnormal: constrictions rarely complete the subdivision of the yolk. Variable heart defects evident as kinked or discontinuous heart. Examination with antibody to the vasa gene product pole cell marker reveal that the shape of the gonads is also abnormal. The adult muscle precursors in the embryo, identified as persistant twist-expressing cells, show variable abnormalities of number and position: up to 25% of the adult muscle precursor cells can be missing.
zfh15 is partially rescued by Scer\GAL4elav-C155/zfh1UAS.cLa
zfh15/zfh175.26 is partially rescued by Scer\GAL4elav-C155/zfh1UAS.cLa
zfh15 is not rescued by Scer\GAL4s.gcm/zfh1UAS.cLa
zfh15/zfh175.26 is not rescued by Scer\GAL4s.gcm/zfh1UAS.cLa
zfh15 and zfh15/zfh175.26 embryos expressing zfh1Scer\UAS.cLa under the control of Scer\GAL4elav-C155 show a substantial rescue in the ability of the ISNb and SNa nerves to exit the CNS, but does not rescue the ISN projection defects.