Suppressor of deltex (
Su(dx)) is a
Drosophila melanogaster member of the NEDD4 family of the HECT domain E3 ubiquitin ligases.
Su(dx) acts as a regulator of Notch endocytic trafficking, promoting Notch lysosomal degradation and the down-regulation of both ligand-dependent and ligand-independent signalling, the latter involving trafficking through the endocytic pathway and activation of the endo/lysosomal membrane. Mutations of
Su(dx) result in developmental phenotypes in the
Drosophila wing that reflect increased Notch signalling, leading to gaps in the specification of the wing veins, and
Su(dx) functions to provide the developmental robustness of Notch activity to environmental temperature shifts. The full developmental functions of
Su(dx) are unclear; however, this is due to a lack of a clearly defined null allele. Here we report the first defined null mutation of
Su(dx), generated by P-element excision, which removes the complete open reading frame. We show that the mutation is recessive-viable, with the Notch gain of function phenotypes affecting wing vein and leg development. We further uncover new roles for
Su(dx) in
Drosophila oogenesis, where it regulates interfollicular stalk formation, egg chamber separation and germline cyst enwrapment by the follicle stem cells. Interestingly, while the null allele exhibited a gain in Notch activity during oogenesis, the previously described
Su(dx)SP allele, which carries a seven amino acid in-frame deletion, displayed a Notch loss of function phenotypes and an increase in follicle stem cell turnover. This is despite both alleles displaying similar Notch gain of function in wing development. We attribute this unexpected context-dependent outcome of
Su(dx)sp being due to the partial retention of function by the intact C2 and WW domain regions of the protein. Our results extend our understanding of the developmental role of
Su(dx) in the tissue renewal and homeostasis of the
Drosophila ovary and illustrate the importance of examining an allelic series of mutations to fully understand developmental functions.
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