dx is a tissue-specific component of the N signal, although its function is not essential for N signaling in any developmental context. dx can both activate and suppress N signaling.

Mutant analysis suggests that dx signalling is dependent on the activity of Su(H).

dx protein activates N signaling in a Su(H)-independent manner. dx protein promotes the relocalisation of N protein from the apical plasma membrane to the intracellular vesicles. The accumulation of N protein in the late endosome appears to be required for dx-mediated Su(H)-independent N signaling.

The dx RING-H2 domain is required for the formation of dx homo-multimer complexes.

Mutations (unspecified) enhance the rough eye phenotype of Ser^{TM.sev.T:VSV\G} and Dl^TM.sev flies.

The dx gene product functions in N signalling as a positive regulator, that acts genetically upstream of N.

Mutations can act as dominant modifiers of the activated N eye phenotype (FBrf0064452).

Genetic interaction analysis suggests a three-way interaction between Su(dx), dx and N.

dx is involved in the N signalling pathway.

Loss of function alleles of Su(H) dominantly suppress wing tip deltas and thick veins phenotype of dx, but gain of function alleles of Su(H) dominantly enhance the phenotype of mutant phenotype of dx causing reduced, vg-like wings.

Su(H) shows allele specific interactions with N, Dl, dx and mam.

Mutations at dx share phenotypes with mutations at sno, and genetic interactions indicate that sno, dx and N function in common pathways.

dx is involved in cell fate decision processes. The dx gene functions with N in one or more developmental pathways to specify cell fate.

dx is a suppressor of N and plays an important role in the genetic circuitry within which N, Dl and mam neurogenic loci operate.

dx mutations are associated with a maternal embryo effect.