nmr2, extra, neuromancer2, lost in space, neuromancer 2
Gene model reviewed during 5.42
Gene model reviewed during 5.52
Click to get a list of regulatory features (enhancers, TFBS, etc.) and gene disruptions (point mutations, indels, etc.) within or overlapping Dmel\mid using the Feature Mapper tool.
In wild-type third instar larvae, mid is ubiquitously expressed in the nucleus in both peripodial epithelium and the disc proper.
mid staining is found only to the posterior of the dorsal appendage forming follicle cells, where br expression is present but much weaker than in the roof cells. It is also not expressed in the br-negative cells on the dorsal midline, between the two patches of roof cells.
mid protein is expressed in a large number of neurons in the ventral midline. It was localized to specific midline neuroblasts at embryonic stages 10 and 11. At stage 13, it was found to be expressed in a row 5 GMC, dubbed an "M-neuron", that appears to change into an extra RP2. It's relation to the NB4-2->GMC-1->RP2/sib lineage is described.
GBrowse - Visual display of RNA-Seq signalsView Dmel\mid in GBrowse 2
Please Note FlyBase no longer curates genomic clone accessions so this list may not be complete
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.
mid is required for the formation and specification of neuroblasts in the anterior-most part of each embryonic segment.
Mutants have an extra RP2 or RP2Sib neuron in the endogenous position as well as an ectopic RP2 neuron at the periphery of the nerve cord.
Mutations in 12 complementation groups differentially affect lateral chordotonal axon growth, fasciculation or ventral orientation. Mutations in robo, spen, sli and los cause lch axon defasciculation. Mutations in sli and los also cause some lch axon bundles to grow dorsally along a trajectory 180o from normal.
mid mutations inhibit the formation of axon tracts between segments of the embryo, sensory axon pathfinding in the PNS and certain tracheal and glial cell migrations.
Mutations in mid generate malformations of the longitudinal tracts.