High impact information on shn

• Genetic epistasis experiments indicate that shn functions downstream of the dpp signal and its receptors [1].
• The shn gene encodes a large protein similar to a family of mammalian zinc finger transcription factors [1].
• Thus, brk inhibition by Shn results in the upregulation of Dpp-responsive genes [2].
• Our results suggest that vertebrate Shn proteins function in Bmp signal transduction, and that Shn proteins recruit coactivators and co-repressors in a context-dependent manner, rather than acting as dedicated activators or repressors [2].
• The zinc-finger transcription factor Schnurri (Shn) has been implicated as a co-factor for Mad, based on its DNA-binding ability and evidence of signaling dependent interactions between the two proteins [3].

Biological context of shn

• We demonstrate that loss of shn activity affects anterior-posterior patterning and cell proliferation in the wing blade, in a manner that reflects the graded requirement for Dpp in these processes [4].
• In this study we investigated the role of the zinc finger transcription factor Schnurri (Shn) in mediating the nuclear response to Dpp during adult patterning [4].
• We find that during embryogenesis, brk expression is derepressed in shn mutants [3].
• Several Dpp target genes are expressed at intermediate levels in double mutant embryos, demonstrating that shn also provides a brk-independent positive input to gene activation [3].
• The Shn-binding sites are relevant for in vivo expression, since mutations in these sites affect the ability of the enhancer to respond to Dpp [5].

Anatomical context of shn

• Mutations in shn affect several developmental processes regulated by dpp including induction of visceral mesoderm cell fate, dorsal/ventral patterning of the lateral ectoderm and wing vein formation [6].
• Mosaic analysis demonstrates that punt and schnurri act within somatic cyst cells that surround germ cells, rather than in germ cells [7].

Physical interactions of shn

• Finally, we found that Shn interacts with Mad in a Dpp-dependent manner [8].

Regulatory relationships of shn

• Furthermore, we find that shn is expressed in the pupal wing and plays a distinct role in mediating dpp-dependent vein differentiation at this stage [4].

Other interactions of shn

• Our data are consistent with a model in which Shn acts as a cofactor for Mad [4].
• punt and schnurri regulate a somatically derived signal that restricts proliferation of committed progenitors in the germline [7].

Analytical, diagnostic and therapeutic context of shn

• By screening for mutants in which daughter cells fail to stop dividing, we find that the TGF-beta signal transducers schnurri and punt are required to limit transient amplification of germ cells [7].
• To examine the relative contribution of the two proteins in the regulation of endogenous Dpp target genes we developed a cell culture assay and show that Shn and Mad act synergistically to induce transcription [5].

References