Gene model reviewed during 5.52
There is only one protein coding transcript and one polypeptide associated with this gene
Efficient DNA binding requires dimerization with another bHLH protein. Interacts with Daughterless (da).
Click to get a list of regulatory features (enhancers, TFBS, etc.) and gene disruptions (point mutations, indels, etc.) within or overlapping Dmel\amos using the Feature Mapper tool.
amos transcripts are expressed transiently and dynamically during embryogenesis. They are present in a small cluster of ectodermal cells in each thoracic and abdominal segment during stage 10. In stage 11, expression is restricted to a single cell in each segment which quickly ceases expression of amos, first in the thorax and then in the abdomen. The restriction of amos expression to a single cell involves lateral inhibition and does not occur in N mutants. amos expression is also observed in developing head segments in the antennal, mandibular, and labial segments in regions corresponding to the anlage for the olfactory sense organs and the larval antennomaxillary complex. amos transcripts are also detected in cellular blastoderm embryos in a dorsoventral band in the posterior of the embryo and during oogenesis in nurse cells, centripetally migrating follicle cells, and in the oocyte. Later in development, amos transcripts are detected at 0-4hr APF in the anlage of the tarsal claw. The main site of later expression is in the antennal disc, initiating at puparium formation. Expression occurs in three semicircular bands on the medial side of the developing third segment. These are sites from which olfactory sensillum precursors are selected.
amos transcripts are ubiquitous before cellularization. The first zygotic expression is detected in clusters of cells in the procephalic region followed by expression in the segments of the head, thorax, and abdomen. Expression is observed in one cluster in each thoracic and abdominal hemisegment and in three clusters in the maxillary and labial hemisegments and in the procephalic region. With time, expression becomes limited within each cluster.
Amos first appears in the third segment of the antennal disc at 1 hr APF. At 2 hr APF, it appears in three to four semicircular domains in the third antennal segment which broaden to appear into a single 'C-shaped' band of cells by 8 hr and 12 hr APF. Its expression partly overlaps that of ems spatially and temporally.
GBrowse - Visual display of RNA-Seq signalsView Dmel\amos 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.
The "Roi" rough eye mutant allele is due to an inversion between 36A and 37A (In(2L)Roi1). The proximal breakpoint is 2.6kb downstream of "amos" and is within the last exon of CG15160. The distal breakpoint is within the first intron of CG5888. Several lines of evidence suggest that the "Roi" phenotype is caused by a gain-of-function allele of "amos" rather than being due to an effect of the inversion on another gene; "amos" is expressed in high levels in a broad area surrounding the morphogenetic furrow in "Roi" third instar larvae (in contrast to wild type), overexpression of "amos" in the eye disc can produce a phenotype similar to that of "Roi" and reversion of the phenotype has been achieved by the insertion of a P-element a few kilobases downstream of "amos" which is associated with a severe reduction of "amos" expression in the eye. In addition, although the location of the In(2L)Roi1 breakpoints means that a chimeric gene could potentially be formed from the 5' portion of CG5888 and the 3' portion of CG15160, this chimeric RNA has not been detected in "Roi" mutants and although dac is also within the inverted segment it does not appear to be implicated in the "Roi" phenotype.
amos is a proneural gene for olfactory sensilla, most likely the sensilla basiconica and trichodea.
Ritterhouse, 25th June 1952. Ives, 18th Nov. 1947.