l(2)br35, l(2)35Da, br35, BG:DS03023.1
zinc finger transcriptional repressor - required in neuroblasts to maintain self-renewal by promoting cell-cycle progression and inhibiting premature differentiation - expressed in the neuroblasts of brain hemispheres and the ventral ganglion - promotes ommatidial death during eye development and subsequent photoreceptor formation - controls both asymmetry and cell division of neuroblasts
Gene model reviewed during 5.52
There is only one protein coding transcript and one polypeptide associated with this gene
Click to get a list of regulatory features (enhancers, TFBS, etc.) and gene disruptions (point mutations, indels, etc.) within or overlapping Dmel\wor using the Feature Mapper tool.
Expression assayed at stages 9, 11, 13, and 17. Expression may be continuous between assayed stages in some tissues.
wor transcript is limited to neural tissues. Embryonic expression is detected at the start of neurogenesis, in two patches of cells anterior to the cephalic furrow. At stage 9, expression is detected in the first wave of delaminating neuroblasts, and in the head region. In the germ band extended embryo, wor transcript is detected in most neuroblasts, in a pattern resembling sna expression. Later in embryogenesis, expression continues to be detected in the brain and ventral nerve cord.
GBrowse - Visual display of RNA-Seq signalsView Dmel\wor 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.
Source for identity of: wor CG4158
dsRNA has been made from templates generated with primers directed against this gene. RNAi of wor results in dorsal overextension of primary dendrites and a reduction in lateral branching. RNAi also causes defects in dendrite morphogenesis and reproducible defects in da dendrite development.
Mutant developing larvae fail to shorten their brainstems.