fs(1)M50, EG:BACR37P7.3 , l(1)G0142
Gene model reviewed during 5.55
Gene model reviewed during 5.46
May be component of a dicistronic gene; available data inconclusive.
Gene model reviewed during 5.54
Low-frequency RNA-Seq exon junction(s) not annotated.
Gene model reviewed during 6.02
601 (aa); 66 (kD)
Click to get a list of regulatory features (enhancers, TFBS, etc.) and gene disruptions (point mutations, indels, etc.) within or overlapping Dmel\cin using the Feature Mapper tool.
GBrowse - Visual display of RNA-Seq signalsView Dmel\cin in GBrowse 2
Please Note This section lists cDNAs and ESTs that fall within the genomic extent of the gene model, which may include cDNAs and ESTs of genes within introns, or of overlapping genes. Please see GBrowse for alignment of the cDNAs and ESTs to the gene model.
For each fully sequenced cDNA the DGRC maintains various forms of the cDNA (e.g tagged or untagged) in several different host vectors for subsequent cloning and expression in Drosophila and Drosophila cell lines.
One of 42 Drosophila genes identified as being most likely to reveal molecular and cellular mechanisms of nervous system development or plasticity relevant to human Mental Retardation disorders.
Affected progeny lack activity for four different molybdenum hydroxylases -- all known to require a molybdenum-containing cofactor for catalytic function. These are aldehyde oxidase, pyridoxal oxidase, xanthine dehydrogenase and sulfite oxidase.
High levels of XDH-CRM (xanthine dehydrogenase cross-reacting material) are found in mutant cin flies. The effects of the mutant gene is on the function of XDH protein rather than its accumulation.
Mutations of cin exhibit no sulfite oxidase activity. Xanthine dehydrogenase and aldehyde oxidase cannot be detected, but there are wild-type levels of alcohol dehydrogenase.
Inactivity of xanthine dehydrogenase accounts for the eye color phenotype. Level of low-molecular-weight molybdenum cofactor severely reduced. cin progeny of cin mothers CRM negative for pyridoxal oxidase.
Mosaic and transplantation analysis indicate that the maternal effect of cin+ on eye color requires the presence of cin+ in the oocyte, whereas cin+ in ovarian mesoderm contributes to the maternal effect on viability.
Four complementation groups described by Baker; a fifth observed by Warner.
The gene was named "cinnamon" by Bruce Baker in 1973 because escapers have dark, brownish eyes. He used the symbol "cin" in order to refer to "the wages of cin".