FlyBase Allele Report: Dmel\trn[28.4]

General Information

Symbol

Dmel\trn^28.4

Species

D. melanogaster

Name

FlyBase ID

FBal0032903

Feature type

allele

Associated gene

Dmel\trn

Associated Insertion(s)

Carried in Construct

Also Known As

trn^25/4

Key Links

Allele class

Mutagen

Delta2-3 transposase

Nature of the Allele

Allele class

Mutagen

Delta2-3 transposase

(Chang et al., 1993)

Progenitor genotype

P{lacW}70A1-2

(Chang et al., 1993)

Cytology

Description

Deletion of between 1.6kb and 1.9kb, beginning in the Ecol\lacZ gene of the progenitor insertion such that 3' P sequences are deleted, together with 1kb of 5' genomic trn DNA and up to between codons 164 and 274 of the trn open reading frame.

(Chang et al., 1993)

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 | embryonic stage (with Df(3L)trn^Δ17)

(Kohsaka and Nose, 2009)

abnormal neuroanatomy | recessive

(Kurusu et al., 2008)

abnormal neuroanatomy | somatic clone

(Hong et al., 2009)

lethal - all die during embryonic stage | recessive

(Chang et al., 1993)

some die during embryonic stage | recessive

(Chang et al., 1993)

Phenotype Manifest In

antennal lobe projection neuron of ALl1 lineage | somatic clone

(Hong et al., 2009)

dendrite | somatic clone

(Hong et al., 2009)

embryonic/larval salivary gland

(Maybeck and Röper, 2009)

larval intersegmental nerve

(Kurusu et al., 2008)

larval intersegmental nerve branch ISNb of A1-7

(Kurusu et al., 2008)

larval segmental nerve branch SNa of A1-7

(Kurusu et al., 2008)

larval somatic muscle cell

(Chang et al., 1993)

motor neuron | embryonic stage (with Df(3L)trn^Δ17)

(Kohsaka and Nose, 2009)

muscle cell of A1-7 dorsal transverse muscle 1 (with In(3LR)C190)

(Artero et al., 2003)

muscle cell of A1-7 lateral transverse muscle 1 (with In(3LR)C190)

(Artero et al., 2003)

muscle cell of A1-7 lateral transverse muscle 2 (with In(3LR)C190)

(Artero et al., 2003)

muscle cell of A1-7 lateral transverse muscle 3 (with In(3LR)C190)

(Artero et al., 2003)

muscle cell of A1-7 lateral transverse muscle 4 (with In(3LR)C190)

(Artero et al., 2003)

presumptive embryonic/larval peripheral nervous system

(Chang et al., 1993)

pretarsus | somatic clone

(Sakurai et al., 2007)

tracheal dorsal trunk primordium

(Krause et al., 2006)

tracheal lateral trunk primordium

(Krause et al., 2006)

Detailed Description

Statement

Reference

Lateral neuroblast clones in the antennal lobe that are homozygous for trn^28.4 result in ectopic innervation of glomeruli that are normally not the targets of lateral projection neurons.

(Hong et al., 2009)

Compared to wild-types, the number of contact points is reduced between myopodia and growth cones in trn^28.4/Df(3L)trn^Δ17 mutant embryos.

(Kohsaka and Nose, 2009)

Invaginating trn^28.4 salivary glands often show irregular lumens.

(Maybeck and Röper, 2009)

trn^28.4 homozygous embryos have motor axon guidance defects that primarily affect the ISNb and SNa nerves including truncation of ISNb prior to muscle 13, failure f the ISNb to branch from the intersegmental nerve and failure of SNa to bifurcate.

(Kurusu et al., 2008)

Homozygous clones in the eye disc appear normal.

(Mao et al., 2008)

Similarly to wild-type clones, trn^28.4 single mutant clones display irregular boundaries.

With regards to trn^28.4 mutant clones in the leg imaginal disc, the displacement rate of cells from tarsal segment 5 to to the pretarsal segment is reduced from the 95.2% in wild-type clones to 80.0% in the mutants.

(Sakurai et al., 2007)

trn^28.4 mutant embryos show gaps in both the dorsal and lateral trunk.

(Krause et al., 2006)

trn^28.4/In(3LR)C190 embryos show a block in normal somatic muscle morphogenesis, without defects in the initial specification of the muscles. Muscles LT1-4 and DT1 often have abnormal shapes and attachments.

(Artero et al., 2003)

Homozygous clones do not cause observable alterations in the wing disc.

(Milan et al., 2001)

Segmentation normal.

(Chang et al., 1993)

External Data

Linkouts

Interactions

Show genetic interaction network for Enhancers & Suppressors

Phenotypic Class

Enhancer of

Statement

Reference

trn^28.4/trn[+] is an enhancer of visible | dominant phenotype of Bx¹

(Bejarano et al., 2008)

trn^28.4/trn[+] is an enhancer of visible phenotype of Bx¹

(Milan et al., 2001)

NOT Enhancer of

Statement

Reference

trn^28.4 is a non-enhancer of abnormal neuroanatomy phenotype of caps^Del1

(Berger-Müller et al., 2013)

Other

Statement

Reference

caps^Del1, trn^28.4 has abnormal neuroanatomy | somatic clone phenotype

(Hong et al., 2009)

Phenotype Manifest In

Enhanced by

Statement

Reference

trn^28.4 has tracheal dorsal trunk primordium phenotype, enhanceable by Scer\GAL4^twi.PG/caps^UAS.cSa

(Krause et al., 2006)

trn^28.4 has tracheal dorsal trunk primordium phenotype, enhanceable by Scer\GAL4^twi.PG/caps^ID.UAS

(Krause et al., 2006)

trn^28.4 has tracheal dorsal trunk primordium phenotype, enhanceable by caps::trn^{trnEd.capsId.UAS}/Scer\GAL4^twi.PG

(Krause et al., 2006)

Suppressed by

Statement

Reference

trn^28.4 has tracheal dorsal trunk primordium phenotype, suppressible | partially by Scer\GAL4^twi.PG/caps^ED.UAS

(Krause et al., 2006)

trn^28.4 has tracheal dorsal trunk primordium phenotype, suppressible | partially by Scer\GAL4^twi.PG/caps::trn^{capsEd.trnId.UAS}

(Krause et al., 2006)

Enhancer of

Statement

Reference

trn^28.4/trn[+] is an enhancer of wing margin phenotype of Bx¹

(Bejarano et al., 2008)

trn^28.4/trn[+] is an enhancer of wing phenotype of CSN5^L4032

(Doronkin et al., 2003)

trn^28.4/trn[+] is an enhancer of wing phenotype of Bx¹

(Milan et al., 2001)

NOT Enhancer of

Statement

Reference

trn^28.4 is a non-enhancer of photoreceptor cell R8 phenotype of caps^Del1

(Berger-Müller et al., 2013)

Other

Statement

Reference

caps^Del1, trn^28.4 has antennal lobe projection neuron of ALl1 lineage | somatic clone phenotype

(Hong et al., 2009)

caps^Del1, trn^28.4 has embryonic/larval salivary gland phenotype

(Maybeck and Röper, 2009)

caps^Del1, trn^28.4 has cone cell phenotype

(Mao et al., 2008)

caps^Del1, trn^28.4 has eye disc | cell non-autonomous phenotype

(Mao et al., 2008)

caps^Del1, trn^28.4 has eye disc morphogenetic furrow | cell non-autonomous phenotype

(Mao et al., 2008)

caps^Del1, trn^28.4 has ommatidium | cell non-autonomous phenotype

(Mao et al., 2008)

Additional Comments

Genetic Interactions

Statement

Reference

caps^Del1 trn^28.4 double mutants do not exhibit an enhanced mutant R8 photoreceptor phenotype compared to caps^Del1 single mutants.

(Berger-Müller et al., 2013)

Lateral neuroblast clones in the antennal lobe that are doubly homozygous for caps^Del1 and trn^28.4 show two types of dendrite targeting defects; loss of innervation in glomeruli that are normally targets of lateral projection neurons and gain of innervation in glomeruli that are normally not the targets of lateral projection neurons. Loss of innervation of the VA7m, VC1 and VC2 glomeruli is frequently seen in the double mutant embryos.

(Hong et al., 2009)

Invaginating caps^Del1 trn^28.4 salivary glands often show irregular lumens.

(Maybeck and Röper, 2009)

trn^28.4 caps^Del1 double mutant clones in the eye disc show subtle but consistent defects. At the clone border, there is a consistent reduction in the apical constriction of cells. This phenotype is fully penetrant, but appears more pronounced when the clone boundary is perpendicular to the morphogenetic furrow. Within the morphogenetic furrow, cells at the clone boundary are also taller than their neighbours, as their apical surfaces are elevated, disrupting the furrow. The phenotypes of relaxation of apical constriction and increase in apical-basal height of cells are non-autonomous as they are seen in both mutant and wild-type cells at the clone boundary. The range of the phenotype is only 2-3 rows of cells beyond the clone border.

trn^28.4 caps^Del1 double mutant clones in the third instar eye disc result in a perturbation in ommatidial spacing. This is only apparent at the boundaries between mutant and wild-type cells, where ommatidia close to these boundaries are often clearly displaced from their normal positions with no obvious change to their individual morphology. The total number of ommatidia is not affected. This phenotype is non-autonomous, with both mutant and wild-type ommatidia showing mis-positioning. At pupal stages of development, spacing defects are still seen in eye discs with trn^28.4 caps^Del1 double mutant clones, and fusion of neighbouring ommatidia that are abnormally close to each other is seen in about 5% of ommatidia adjacent to clone boundaries. Very occasional defects are seen in the number of cone cells.

(Mao et al., 2008)

trn^28.4, caps^65.2 double mutant embryos show an additive phenotype, where the sum of the gaps in the dorsal and lateral trunks seen in single mutants is close to the figure seen in the double mutants.

Expression of caps^ED.Scer\UAS under the control of Scer\GAL4^twi.PG in trn^28.4 embryos rescues the dorsal trunk defects in 47% of cases. In contrast, expression of either caps^Scer\UAS.cSa or caps^ID.Scer\UAS, under the control of Scer\GAL4^twi.PG, increases the severity of the dorsal trunk formation trn^28.4 phenotype.

Expression of caps::trn^{capsEd.trnId.Scer\UAS} under the control of Scer\GAL4^twi.PG rescues the tracheal defects of trn^28.4 embryos. In contrast, expression of caps::trn^{trnEd.capsId.Scer\UAS} under the control of Scer\GAL4^twi.PG enhances the tracheal defects of trn^28.4 embryos so that these embryos show 11.2% more dorsal trunk interruptions than trn^28.4 mutants.

(Krause et al., 2006)

Xenogenetic Interactions

Statement

Reference

Complementation and Rescue Data

Rescued by

trn^28.4 is rescued by Scer\GAL4^twi.PG/trn^UAS.cMa

(Krause et al., 2006)

trn^28.4 is rescued by Scer\GAL4^twi.PG/trn^{ΔC.UAS.Tag:MYC}

(Krause et al., 2006)

Comments

Images (0)

Mutant

Wild-type

Stocks (0)

Notes on Origin

Discoverer

External Crossreferences and Linkouts ( 0 )

Synonyms and Secondary IDs (3)

Reported As

Symbol Synonym

trn^25.4

(Artero et al., 2003)

trn^25/4

(Kohsaka and Nose, 2009, Bejarano et al., 2008, Milan et al., 2001)

trn^28.4

(Sharrock et al., 2022, Berger-Müller et al., 2013, Hong et al., 2009, Hong et al., 2009, Maybeck and Röper, 2009, Kurusu et al., 2008, Mao et al., 2008, Sakurai et al., 2007, Krause et al., 2006)

Name Synonyms

Secondary FlyBase IDs

References (16)

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