|Feature type||allele||Associated gene||Dmel\rst|
|Also Known As||rstCT|
|Allele class||loss of function allele|
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|Nature of the Allele|
|Mutations Mapped to the Genome|
|Associated Sequence Data|
|Nature of the lesion|
Disrupts the intracellular domain.
98bp deletion that severely affects the cytoplasmic domain.
Polytene chromosomes normal.
Polytene chromosomes normal.
|Phenotype Manifest In|
Hemizygous rst retinas exhibit supernumerary inter-ommatidial pigment cells (IPCs) that are poorly patterned. The IPCs do not undergo the normal cell intercalation that would produce a single layer of cells between ommatidia. These cells have the ability and tendency toward movement. However, these movements are undirected and hence there is no resolution of the IPC lattice into a single layer of cells. The undirected cell movements continue through at least 24-28 hours a.p.f. Primary pigment cell precursors are properly differentiated, but during their early development, the primary pigment cells tend to abnormally contact each other. However, most of these contacts are resolved over time.
In rst/Y animals, rearrangement of adherens junctions between inter-ommatidial precursor cells from 18-31 hours APF is partially disrupted, as is arrangement of these cells into an orderly array.
In the eye disc of hemizygous rst6 flies, cell sorting does not occur, leading to an excess of surviving interommatidial precursor cells. In contrast, rst6/+ eye discs display no strong sorting defects and only occasionally have supernumerary interommatidial precursor cells.
In the developing eyes of hbs[IR.Scer\UAS]; Scer\GAL4[GMR.PF] animals at 24 hours APF, ommatidial cores are largely normal, but inter-ommatidial precursor cells (IPCs) fail to sort into a single line as in wild-type; subsequent patterning steps of these cells are arrested. By 30 hours APF, these cells have abnormally large apical profiles and fail to form typically scalloped contacts with primary pigment cells or to minimize contacts with neighboring inter-ommatidial cells. Cell junctions still form between primary precursors and IPCs, although the normal polarization of some junction components is disrupted. In more mature eyes, 3 or more cells often share a single tertiary pigment cell niche and interommatidial bristle precursors fail to move to their correct location. The result is a rough adult eye phenotype due to disorganized arrangement of ommatidia. In the developing eyes rst/+ animals at 42 hours APF, the arrangement of inter-ommatidial precursors is mildly disrupted: most commonly, 2 cells occupy a single tertiary pigment (3') cell niche (17% of 3' niches); occasionally, secondary pigment cells invade a tertiary niche.
Mutant pupal eye discs do not show elimination of surplus interommatidial (lattice) cells (which occurs in wild-type discs) and disruption of cell sorting is seen.
Homozygous muscles show thin muscles and sometimes lack muscles entirely in some segments. Furthermore, embryos exhibit muscles in ectopic positions.
Many ectopic interommatidial bristles are visible throughout the interommatidial lattice in mature mutant pupal retinas. Adult eyes have a rough surface with misaligned ommatidial rows.
The total number of sensilla on the antenna are comparable to wild-type controls, but spacing between adjacent sensilla is altered and there are regions where the sense organs appear in tufts. Clusters of 6 to 8 sensilla basiconica often appear to fall into a pit in the epidermis. The total number of sensory founder cells in the antennal disc is comparable to wild type, but the pattern of the founder cells is disorganised. The pattern of apoptotic nuclei in third larval instar antennal discs is no different from wild type.
Severe eye phenotype.
Rough eye phenotype.
Occasional extra secondary pigment cells within the eye. Low levels of cell death are seen in the larval eye disc leading to a disorganised retinal lattice.
Spacing of arcs along the posterior of the morphogenetic furrow appears normal.
No defects in optic chiasm.
Timing of adult emergence is normal.
viability normal in both sexes no vt effect
|Phenotype Manifest In|
rst6/rst[+] is an enhancer of inter-ommatidial precursor cell | supernumerary | pupal stage phenotype of Scer\GAL4GMR.PF, pyd3.dsRNA.Scer\UAS
rst6 is a suppressor of ommatidium phenotype of Scer\GAL4GMR.PF/Scer\GAL4GMR.PF, cindrdsRNA.PC.PD.Scer\UAS
rst6 is a suppressor of pigment cell phenotype of Scer\GAL4GMR.PF/Scer\GAL4GMR.PF, cindrdsRNA.PC.PD.Scer\UAS
rst6 is a suppressor of primary pigment cell phenotype of Scer\GAL4GMR.PF/Scer\GAL4GMR.PF, cindrdsRNA.PC.PD.Scer\UAS
rst6 is a suppressor of secondary pigment cell phenotype of Scer\GAL4GMR.PF/Scer\GAL4GMR.PF, cindrdsRNA.PC.PD.Scer\UAS
Pupae heterozygous for rst exhibit mild but consistent suppression of the Scer\GAL4[GMR.PF]>cindr[dsRNA.PC.PD.Scer\UAS] phenotype. The prevalence of cone and 1[o] cell defects is decreased and the number of 2[o] and 3[o] cells is reduced to slightly below normal.
Expression of Scer\GAL4[GMR.PF] driven α-Cat[Scer\UAS.T:Avic\GFP-sg] leads to a mild enhancement of some of the rst pupal retina phenotypes.
One copy of rst strongly enhances the increase in inter-ommatidial precursor cell number seen when pyd[3.dsRNA.Scer\UAS] is expressed under the control of Scer\GAL4[GMR.PF].
Expression of one copy of X11LdsRNA.Scer\UAS, driven by Scer\GAL4GMR.PF, in a rst6/+ background leads to severe cell sorting defects in eye discs, similar to those seen in rst6 homozygotes.
The mild defects in the arrangement of inter-ommatidial precursor cells seen in rst/+ animals at 42 hours APF are enhanced by hbs/+: the percentage of abnormal tertiary pigment cell niches is increased from 17-37% with some niches completely lacking a tertiary pigment cell. In addition, inter-ommatidial bristles are occasionally missing and some secondary pigment cells have abnormal morphology.
|Complementation & Rescue Data|
|Stocks ( 4 )|
|Notes on Origin|
|External Crossreferences & Linkouts|
|Synonyms & Secondary IDs ( 6 )|
(Vishnu et al., 2005, Dworak et al., 2001, Frohlich, 2001, Reddy et al., 1999, Reiter et al., 1996, Araujo et al., 1996, Schneider et al., 1995, Ramos et al., 1993, Ramos et al., 1993, Ramos et al., 1991, Wolff and Ready, 1991, Wolff and Ready, 1991, Ramos et al., 1991, Boschert et al., 1990, Welshons and Welshons, 1986, Vishnu et al., 2006, Simon et al., 2009, Bao and Cagan, 2005, Cordero et al., 2007, Larson et al., 2008, Johnson et al., 2008, Seppa et al., 2008)
|Secondary FlyBase IDs|
|References ( 33 )|
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|Recent research papers (0)|
|All research papers listed in FlyBase were published before 2011|