FlyBase Allele Report: Dmel\rst[6]

General Information

Symbol

Dmel\rst⁶

Species

D. melanogaster

Name

FlyBase ID

FBal0014797

Feature type

allele

Associated gene

Dmel\rst

Associated Insertion(s)

Carried in Construct

Also Known As

rst^CT

Key Links

Allele class

loss of function allele

Mutagen

ethyl methanesulfonate

Nature of the Allele

Allele class

loss of function allele

(Johnson et al., 2008, Larson et al., 2008)

Mutagen

ethyl methanesulfonate

(Wolff and Ready, 1991, Lefevre and Green, 1972)

Progenitor genotype

Cytology

Polytene chromosomes normal.

(Lefevre and Green, 1972)

Description

rst⁶ is a truncation mutant.

(Larson et al., 2008)

Disrupts the intracellular domain.

(Ramos et al., 1993)

98bp deletion that severely affects the cytoplasmic domain.

(Ramos et al., 1993)

Point mutant.

(Welshons and Welshons, 1986)

Mutations Mapped to the Genome

Curation Data

Type

Location

Additional Notes

References

Variant Molecular Consequences

Associated Sequence Data

DDBJ / EMBL / GenBank

DNA sequence

Protein sequence

UniProtKB/Swiss-Prot

UniProtKB/TrEMBL

Expression Data

Reporter Expression

Additional Information

Statement

Reference

Marker for

Reflects expression of

Reporter construct used in assay

Human Disease Associations

Disease Ontology (DO) Annotations

Models Based on Experimental Evidence ( 0 )

Disease

Evidence

References

Modifiers Based on Experimental Evidence ( 0 )

Disease

Interaction

References

Comments on Models/Modifiers Based on Experimental Evidence ( 0 )

Disease-implicated variant(s)

Phenotypic Data

Phenotypic Class

abnormal neuroanatomy

(Larson et al., 2008)

viable

(Blackie et al., 2021)

visible | recessive

(Tanenbaum et al., 2000)

Phenotype Manifest In

adherens junction

(Cordero et al., 2007)

antennal disc

(Reddy et al., 1999)

antennal segment 3 sense organ

(Reddy et al., 1999)

basiconic sensillum of antennal segment 3

(Reddy et al., 1999)

cell-cell junction

(Bao and Cagan, 2005)

cone cell | P-stage | somatic clone

(Blackie et al., 2021)

embryonic somatic muscle cell | ectopic

(Strunkelnberg et al., 2001)

eye

(Bao and Cagan, 2005)

eye disc

(Grzeschik and Knust, 2005)

interommatidial bristle | ectopic

(Tanenbaum et al., 2000)

interommatidial cell | increased number

(Larson et al., 2008)

interommatidial precursor cell | pupal stage P6

(Cordero et al., 2007)

interommatidial precursor cell | pupal stage P7

(Bao and Cagan, 2005)

ommatidial precursor cluster

(Vishnu et al., 2006)

ommatidium

(Bao and Cagan, 2005, Tanenbaum et al., 2000)

presumptive embryonic/larval muscle system

(Strunkelnberg et al., 2001)

primary pigment cell

(Larson et al., 2008)

Detailed Description

Statement

Reference

Hemizygous rst⁶ 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.

(Larson et al., 2008)

In rst⁶/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.

(Cordero et al., 2007)

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.

(Vishnu et al., 2006)

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 rst⁶/+ 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.

(Bao and Cagan, 2005)

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.

(Grzeschik and Knust, 2005)

Homozygous muscles show thin muscles and sometimes lack muscles entirely in some segments. Furthermore, embryos exhibit muscles in ectopic positions.

(Strunkelnberg et al., 2001)

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.

(Tanenbaum et al., 2000)

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.

(Reddy et al., 1999)

Severe eye phenotype.

(Reiter et al., 1996)

Rough eye phenotype.

(Ramos et al., 1993)

Individuals homozygous for Bpt¹ and rst⁶ exhibit no Bpt¹ phenotype.

(Duus et al., 1992)

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.

(Wolff and Ready, 1991)

Spacing of arcs along the posterior of the morphogenetic furrow appears normal.

(Wolff and Ready, 1991)

No defects in optic chiasm.

(Boschert et al., 1990)

e(fa^swb)¹ rst⁶ flies have slightly rough eyes.

(Welshons and Welshons, 1986)

Timing of adult emergence is normal.

(Lefevre and Green, 1972)

viability normal in both sexes no vt effect

External Data

Linkouts

Interactions

Show genetic interaction network for Enhancers & Suppressors

Phenotypic Class

Enhanced by

Statement

Reference

rst⁶ has abnormal neuroanatomy phenotype, enhanceable by α-Cat^UAS.sgGFP/Scer\GAL4^GMR.PF

(Larson et al., 2008)

Enhancer of

Statement

Reference

rst⁶/rst[+] is an enhancer of increased cell number | pupal stage phenotype of Scer\GAL4^GMR.PF, pyd^RNAi.3.UAS

(Seppa et al., 2008)

Suppressor of

Statement

Reference

rst⁶ is a suppressor of abnormal planar polarity phenotype of Scer\GAL4^GMR.PF, cindr^{RNAi.PC.PD.UAS}

(Johnson et al., 2008)

Phenotype Manifest In

Enhanced by

Statement

Reference

rst⁶ has ommatidial precursor cluster phenotype, enhanceable by Scer\GAL4^MZ1369/X11L^RNAi.UAS

(Vishnu et al., 2006)

rst⁶ has interommatidial precursor cell | pupal stage P7 phenotype, enhanceable by hbs²⁵⁹³/hbs[+]

(Bao and Cagan, 2005)

Enhancer of

Statement

Reference

rst⁶/rst[+] is an enhancer of interommatidial precursor cell | pupal stage | increased number phenotype of Scer\GAL4^GMR.PF, pyd^RNAi.3.UAS

(Seppa et al., 2008)

rst⁶/rst[+] is an enhancer of ommatidial precursor cluster phenotype of Scer\GAL4^GMR.PF, X11L^RNAi.UAS

(Vishnu et al., 2006)

Suppressor of

Statement

Reference

rst⁶ is a suppressor of primary pigment cell phenotype of Scer\GAL4^GMR.PF, cindr^{RNAi.PC.PD.UAS}

(Johnson et al., 2008)

rst⁶ is a suppressor of ommatidium phenotype of Scer\GAL4^GMR.PF, cindr^{RNAi.PC.PD.UAS}

(Johnson et al., 2008)

rst⁶ is a suppressor of pigment cell phenotype of Scer\GAL4^GMR.PF, cindr^{RNAi.PC.PD.UAS}

(Johnson et al., 2008)

rst⁶ is a suppressor of secondary pigment cell phenotype of Scer\GAL4^GMR.PF, cindr^{RNAi.PC.PD.UAS}

(Johnson et al., 2008)

rst⁶ is a suppressor of tertiary pigment cell phenotype of Scer\GAL4^GMR.PF, cindr^{RNAi.PC.PD.UAS}

(Johnson et al., 2008)

Other

Statement

Reference

hbs²⁵⁹³/hbs[+], rst⁶ has interommatidial bristle | pupal stage P7 phenotype

(Bao and Cagan, 2005)

e(fa^swb)¹, rst⁶ has eye phenotype

(Welshons and Welshons, 1986)

Additional Comments

Genetic Interactions

Statement

Reference

The muscle pattern of rst⁶ dock⁰⁴⁷²³ embryos is similar to that of rst⁶ single mutants.

(Kaipa et al., 2013)

Pupae heterozygous for rst⁶ 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.

(Johnson et al., 2008)

Expression of Scer\GAL4^GMR.PF driven α-Cat^{Scer\UAS.T:Avic\GFP-sg} leads to a mild enhancement of some of the rst⁶ pupal retina phenotypes.

(Larson et al., 2008)

One copy of rst⁶ 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.

(Seppa et al., 2008)

Expression of one copy of X11L^{dsRNA.Scer\UAS}, driven by Scer\GAL4^GMR.PF, in a rst⁶/+ background leads to severe cell sorting defects in eye discs, similar to those seen in rst⁶ homozygotes.

(Vishnu et al., 2006)

The mild defects in the arrangement of inter-ommatidial precursor cells seen in rst⁶/+ animals at 42 hours APF are enhanced by hbs²⁵⁹³/+: 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.

(Bao and Cagan, 2005)

Xenogenetic Interactions

Statement

Reference

Complementation and Rescue Data

Comments

Images (1)

Holtzman, S. and Kaufman, T. (2013)

Mutant

Wild-type

Stocks (4)

Bloomington

1528

gt^Q292 rst⁶/FM7a

1530

y¹ gt^E6 rst⁶

Kyoto

106368

gt^Q292 rst⁶/FM7a

106370

y¹ gt^E6 rst⁶

Notes on Origin

Discoverer

External Crossreferences and Linkouts ( 0 )

Synonyms and Secondary IDs (6)

Reported As

Symbol Synonym

irreC-rst^CT

(Tanenbaum et al., 2000)

irreC^CT

(Grzeschik and Knust, 2005)

rst^16172.646

(Lefevre and Green, 1972)

rst⁶

(Lee et al., 2023, Blackie et al., 2021, Kaipa et al., 2013, Popodi et al., 2010-, Christensen et al., 2008.6.11, Christensen et al., 2008.12.28, Christensen et al., 2008.12.28, Christensen et al., 2008.12.28)

rst^ct

(Duus et al., 1992)

Name Synonyms

Secondary FlyBase IDs

References (37)

Report Sections

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