Hairless (H) encodes the major antagonist in the Notch signaling pathway, which governs cellular differentiation of various tissues in
Drosophila. By binding to the Notch signal transducer Suppressor of Hairless (Su(H)), H assembles repressor complexes onto Notch target genes. Using genome engineering,
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Hairless (H) encodes the major antagonist in the Notch signaling pathway, which governs cellular differentiation of various tissues in
Drosophila. By binding to the Notch signal transducer Suppressor of Hairless (Su(H)), H assembles repressor complexes onto Notch target genes. Using genome engineering, three new
H alleles,
HFA,
HLLAA and
HWA were generated and a phenotypic series was established by several parameters, reflecting the residual H-Su(H) binding capacity. Occasionally, homozygous
HWA flies develop to adulthood. They were compared with the likewise semi-viable
HNN allele affecting H-Su(H) nuclear entry. The
H homozygotes were short-lived, sterile and flightless, yet showed largely normal expression of several mitochondrial genes. Typical for
H mutants, both
HWA and
HNN homozygous alleles displayed strong defects in wing venation and mechano-sensory bristle development. Strikingly, however,
HWA displayed only a loss of bristles, whereas bristle organs of
HNN flies showed a complete shaft-to-socket transformation. Apparently, the impact of
HWA is restricted to lateral inhibition, whereas that of
HNN also affects the respective cell type specification. Notably, reduction in
Su(H) gene dosage only suppressed the
HNN bristle phenotype, but amplified that of
HWA. We interpret these differences as to the role of H regarding Su(H) stability and availability.
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