Disease relevance of retn

• Males mutant for retn court with normal parameters, although feminization of retn cells in males induces bisexuality [1].
• Disruption of the spatial organization of the dri-expressing longitudinal glia accounts for the mild defects in axon fasciculation observed in the mutant embryos [2].

High impact information on retn

• In contradiction to this simple model, we show that dsx, as well as fruM and non-sex-specific retained (retn), affect both male and female sexual behaviors [3].
• Thus, we show that fru and dsx together act as a 'switch' system regulating behavior in the context of other developmental genes, such as retn [3].
• Molecularly, retn seems to regulate sexual behavior via a previously described complex that represses zerknullt [3].
• Using NMR spectroscopy, we have determined the first ever three-dimensional structure of an ARID--DNA complex (mol. wt 25.7 kDa) formed by Dead ringer from Drosophila melanogaster [4].
• The Dead ringer protein from Drosophila melanogaster is a transcriptional regulatory protein required for early embryonic development [5].

Biological context of retn

• This subfamily exhibits an extended region of sequence similarity beyond the core ARID motif and a separate conserved domain termed the REKLES domain. retn/dri is involved in a range of developmental processes, including axis patterning and muscle development [6].
• Gel retardation and optimal binding site screens revealed that the in vitro sequence specificity of DRI is strikingly similar to that of many homeodomain proteins, although the sequence and predicted secondary structure do not resemble a homeodomain [7].
• Consistent with the mutant phenotype and the sequence-specific DNA-binding properties of its product, dri was found to be essential for the normal early embryonic expression pattern of several key regulatory genes [8].
• This study establishes dri as an essential co-factor in the regulated expression of specific patterning genes during early embryogenesis [8].
• This suggests that loco and pros are targets of DRI transcriptional activation in some LG [2].

Anatomical context of retn

• Neural defects of retn mutant cells include mushroom body beta-lobe fusion and pathfinding errors by photoreceptor and subesophageal neurons [1].
• Maternally derived dri product is found throughout the embryo until germ band extension, when dri is expressed in a developmentally regulated set of tissues, including salivary gland ducts, parts of the gut, and a subset of neural cells [7].
• We show here that dri is expressed in a subset of longitudinal glia in the Drosophila embryonic central nervous system and that dri forms part of the transcriptional regulatory cascade required for normal development of these cells [2].

Associations of retn with chemical compounds

• In order to quantitatively determine how ARIDs alter their mobility to recognize DNA, we have measured the relaxation parameters of the backbone nitrogen-15 nuclei of Dead ringer in its free and bound forms, and interpreted these data using the model-free approach [9].

Other interactions of retn

• In dri mutant embryos, expression of argos in the terminal domains was severely reduced, accounting for the dri mutant head phenotype [8].
• Gro is recruited to the enhancer element in the vicinity of DI by sequence-specific transcription factors such as Dead Ringer (Dri) [10].

References