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FB2026_02
,
released June 18, 2026
diss, Bj6, no-on-transient A, non-A, dissonance
Please see the JBrowse view of Dmel\nonA for information on other features
To submit a correction to a gene model please use the Contact FlyBase form
AlphaFold produces a per-residue confidence score (pLDDT) between 0 and 100. Some regions with low pLDDT may be unstructured in isolation.
Low-frequency RNA-Seq exon junction(s) not annotated.
Gene model reviewed during 5.50
4.0, 3.0, 2.8 (northern blot)
82 (kD)
80 (kD)
82 (kD observed)
form II
form I
Click to get a list of regulatory features (enhancers, TFBS, etc.) and gene disruptions (point mutations, indels, etc.) within or overlapping Dmel\nonA using the Feature Mapper tool.
The testis specificity index was calculated from modENCODE tissue expression data by Vedelek et al., 2018 to indicate the degree of testis enrichment compared to other tissues. Scores range from -2.52 (underrepresented) to 5.2 (very high testis bias).
During oogenesis, observed in nuclei of follicle cell, nurse cells, and the oocyte. In embryos, observed in nuclei of cells at cellular blastoderm; expressed throughout embryonic development. In larval salivary glands, localized to polytene chromosomes.
@FBgn0004227:nonA @ is nuclear except in early embryos prior to cellular blastoderm stage where it is cytoplasmic.
Comment: low expression throughout adult brain
JBrowse - Visual display of RNA-Seq signals
View Dmel\nonA in JBrowse1-53
1-54.5
1-52
1-56
1-52.3
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 JBrowse 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.
monoclonal
polyclonal
Dissection of the functional domains of nonA.
"Gene order: In direction of increasing cytology: Cyp1- nonA?" was stated as revision.
The RRM motifs of nonA have been analysed by in vitro mutagenesis. RRM1 mutants cause optomotor blindness and an absence of transient spikes in the ERG. RRM2 mutants cause mildly mutant song pulses and trains.
Spatial distribution of nonA protein was followed by confocal laser scanning microscopy in the nuclei of living cells throughout embryogenesis. Active uptake of nonA protein from cytoplasm to nucleus was observed from nuclear cycle 14 onwards. Significant differences between the distribution in fixed and living embryos were noted. The nonA protein was localized in the nuclei of living embryos at discrete sites, mostly at the periphery and sometimes tightly clustered. Observations suggest that specific protein complexes are mobile and associate with active interphase chromatin.
A sequence comparison and numerical analysis of the RRM-containing (RNA recognition motif) proteins suggests that functionally related RRM-containing proteins have significant sequence similarities in their RRMs.
Germline clonal analysis demonstrates that nonA has an essential function in the female germline.
Murine NonO is homologous to nonA, essential for visual processing.
Mutants exhibit defective courtship song.
Expression patterns and nonA protein structure have been determined.
nonA locus has been molecularly cloned, mRNA transcripts characterized and nonA mutant phenotypes rescued by P element mediated transformation.
nonA has been cloned and sequenced and its expression pattern has been analysed.
Mosaic analysis (Hotta and Benzer, 1970) suggested that ERG defects map to photoreceptors; but too few gynandromorphs were analyzed to rule out an optic-lobe 'focus', which is more likely to be the focus for visual-movement-response abnormalities (especially those reported by Heisenberg, 1972). Two genomic clones, whose distal endpoints are just distal to nonA-rescuing DNA fragments, rescue each of two non-allelic lethals <up>l(1)14Cc and l(1)14Ca</up> that map to the same cytogenetic interval as does nonA; transformation with overlapping genomic clones indicates an order from left to right of l(1)14Cc l(1)14Ca nonA (Jones and Rubin, 1990). Both lethals complement the ERG defects of nonA5 (Jones and Rubin, 1990) and complement the song abnormality of nonA9 (Kulkarni and Hall, unpublished).
Defective optomotor responses and phototaxis, with the former being especially defective (Heisenberg, 1972; Heisenberg and Buchner, 1977; Kulkarni, Steinlauf and Hall, 1988). Poor orientation behavior in Y-maze (Bulthoff, 1982). nonA5 flies exhibit specific lack of responses to front-to-back moving visual stimuli, whereas reaction to back-to-front motion is intact (Heisenberg, 1972). Physiologically, there are reduced or absent light-on and light-off transient spikes in electroretinogram, whereas photoreceptor potential is normal (Hotta and Benzer, 1970; Pak, Grossfield and Arnold, 1970; Heisenberg, 1971; Kulkarni, Steinlauf and Hall, 1988; Jones and Rubin, 1990). Larval visual response (re negative phototaxis) normal (Hotta and Keng, 1984). Courtship song is abnormal, as influenced by one, possibly two, mutant alleles; nonA9 (originally diss) males produce abnormal song, regarding pulses relatively late in trains of such song sounds (each one resulting from a bout of wing vibration); the abnormalities are polycyclicity (Kulkarni, Steinlauf and Hall, 1988) and anomalous intra-pulse frequency components (Wheeler et al., 1989); pulses early in trains, or throughout short ones, are nearly normal; courtship hum sounds manifest irregular sine waves, though their fundamental frequencies are normal (Wheeler et al., 1989). nonA9 by itself is also an optomotor-defective/ERG-abnormal mutant (Kulkarni et al., 1988) and fails to complement other mutant alleles with regard to these visual phenotypes (Rendahl, Jones, Kulkarni, Bagully and Hall, 1992); but these heterozygotes, in a homozygous tra genetic background, sing normally (with the possible exception of nonA2/nonA9, Rendahl et al., 1992), as do males hemizygous for alleles isolated as visual mutants.
