Smg1, rst(1a)cyr, Smg
Gene model reviewed during 5.39
Gene model reviewed during 5.52
Component of a post-splicing multiprotein NMD complex.
Click to get a list of regulatory features (enhancers, TFBS, etc.) and gene disruptions (point mutations, indels, etc.) within or overlapping Dmel\nonC using the Feature Mapper tool.
GBrowse - Visual display of RNA-Seq signalsView Dmel\nonC 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 merge of: Smg1 anon-WO0170980.133
Source for merge of: Smg1 anon- EST:Liang-1.24
Source for merge of: Smg1 rst(1a)cyr
Source for merge of: nonC Smg1
Annotations CG4549 and CG4555 merged as CG32743 in release 3 of the genome annotation.
Source for merge of Smg1 anon-WO0170980.133 was sequence comparison ( date:051113 ).
Source for merge of CG4549 CG4555 was a shared cDNA ( date:010720 ).
Loss of nonC function impairs basal synaptic efficacy and reduces the fidelity of neurotransmission.
nonC facilitates gross neuromuscular junction synaptic morphological development, but does not appear to be required for maintenance of pre- and postsynaptic molecular specializations in individual boutons.
nonC is involved in regulation of the trafficking underlying synaptic vesicle pools.
nonC mutants exhibit impaired presynaptic function at the level of whole animal and single synaptic boutons.
Loss of nonC prevents the synaptic vesicle cycle from maintaining the rate required during periods of demand for high-frequency transmission.
dsRNA made from templates generated with primers directed against this gene tested in RNAi screen for effects on Kc167 and S2R+ cell morphology.
Mutants show resistance to cyromazine growth regulator.
Defective phototaxis and optomotor responses; no light-on or light-off transients in electroretinogram, probably due to defect in photoreceptor cells per se; abnormal orientation to spots in Y-maze test.