FlyBase Allele Report: Dmel\dlg1[7]

General Information

Symbol

Dmel\dlg1⁷

Species

D. melanogaster

Name

FlyBase ID

FBal0002676

Feature type

allele

Associated gene

Dmel\dlg1

Associated Insertion(s)

Carried in Construct

Also Known As

dlg^XI-2, dlg^X1-2, l(1)d.lg-1^xi-2

Key Links

Genomic Maps

JBrowse

Allele class

hypomorphic allele - genetic evidence

loss of function allele

Mutagen

ethyl methanesulfonate

Nature of the Allele

Allele class

hypomorphic allele - genetic evidence

(Tejedor et al., 1997)

loss of function allele

Mutagen

ethyl methanesulfonate

(Hanratty and Dearolf, 1993, Woods and Bryant, 1989)

Progenitor genotype

Cytology

Description

Molecular alteration of the protein (new splice acceptor site at the beginning of exon 9) causing a splicing defect that results in a 134bp insertion in exon 9 and a truncated protein.

(Woods et al., 1996)

Mutations Mapped to the Genome

Curation Data

Type

Location

Additional Notes

References

point_mutation

X:11,399,741..11,399,741 [+]

Nucleotide change:

G11399741A

Reported nucleotide change:

G?A

Comment:

A new splice acceptor site, G to A transition, at the beginning of the exon causes a splicing defect that results in a 134bp insertion in the exon and a truncated protein.

(Woods et al., 1996)

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

Phenotype Manifest In

bouton

(Thomas et al., 1997, Thomas et al., 1997)

embryonic/larval brain

(Poodry and Woods, 1990)

embryonic/larval optic lobe

(Woods and Bryant, 1989)

imaginal disc

(Thomas et al., 1997, Woods et al., 1996, Woods and Bryant, 1989)

imaginal disc | larval stage

(Sehnal and Bryant, 1993)

larval ventral nerve cord | larval stage

(Woods and Bryant, 1989)

mesothoracic leg disc | larval stage

(Woods and Bryant, 1989)

neuromuscular junction

(Koh et al., 1999)

neuromuscular junction & bouton

(Koh et al., 1999)

neuromuscular junction & postsynaptic membrane

(Koh et al., 1999)

neuromuscular junction | larval stage

(Mendoza-Topaz et al., 2008)

NMJ bouton

(Zhang et al., 2007)

postsynaptic membrane

(Thomas et al., 1997)

postsynaptic membrane & neuromuscular junction | larval stage

(Mendoza-Topaz et al., 2008)

presynaptic membrane & neuromuscular junction | larval stage

(Mendoza-Topaz et al., 2008)

prothoracic leg disc | larval stage

(Woods and Bryant, 1989)

subsynaptic reticulum

(Zhang et al., 2007)

wing disc | larval stage

(Woods and Bryant, 1989)

Detailed Description

Statement

Reference

There is a significant increase in the length of each pre-synaptic density at larval neuromuscular junctions (NMJs) in dlg1⁷ homozygotes compared to wild-type. However, the thickness of the sub-synaptic reticulum at these NMJs is significantly decreased.

Electrophysiological readings from the neuromuscular junctions of dlg1⁷ homozygotes show significantly increased mini excitatory junction potential amplitude and significantly decreased evoked excitatory junction potential amplitude compared to controls. Together these indicate decreased quantal content.

(Mendoza-Topaz et al., 2008)

Homozygotes show a severe decrease in the number of boutons at the neuromuscular junction compared to controls. The subsynaptic reticulum is less developed in the mutant boutons than in control boutons.

The amplitude of the miniature and evoked excitatory junctional currents are reduced compared to controls in mutant animals. The frequency of the miniature excitatory junctional current and the quantal content are not significantly altered.

(Zhang et al., 2007)

Mutants show defects at the larval neuromuscular junction (NMJ); boutons are enlarged and abnormal NMJ arbors are seen. There is a reduction in the subsynaptic reticulum and an increase in the number of active zones.

(Koh et al., 1999)

Follicle cells do not have an invasive phenotype in females with homozygous dlg1⁷ clones in the germ cells and follicle cells.

(Goode and Perrimon, 1997)

Type Ib boutons at the neuromuscular junction appear bloated.

(Thomas et al., 1997)

The subsynaptic reticulum at type I boutons is greatly reduced in hemizygous flies, such that it fails to surround the type I boutons or forms very few folds at the junctional region. There is an increase in the number of active zones within single type I boutons. The presynaptic terminal of type I boutons is larger in cross-sectional area in hemizygous flies compared to wild-type. The increased number of active zones is completely rescued if dlg1^Scer\UAS.cBa is targeted to the presynaptic cell or simultaneously to both pre- and postsynaptic cells using Scer\GAL4^unspecified. The presynaptic morphological phenotype is partially rescued if dlg1^Scer\UAS.cBa is targeted only to the postsynaptic cell using Scer\GAL4^unspecified.

(Thomas et al., 1997)

Homozygous larval show overgrowth of the imaginal discs. Imaginal disc cells have apical junctions and exhibit normal apicobasal polarity.

(Woods et al., 1996)

Neoplastic imaginal disc overgrowth, affecting all discs. Discs implanted into wild type hosts for metamorphosis overgrow and do not differentiate. Mutant larvae grow at a normal rate until end of feeding period of last larval instar, when growth slows and then stops: they eventually reach double the weight of wild type pupariating larvae. Pupariation delay can be prevented by γ irradiation (destroying proliferating cells) shortly before hatching (Poodry and Woods, Wilhelm Roux's Arch 199:219--227 ). Ecdysteroid titer for all mutants fails to show peak that is associated with pupariation in the wild type. The ecdysteroid secretory activity of dlg1 and l(3)dco ring glands in vitro is 1/6 that of wild type. When overgrowth of the imaginal discs is prevented by γ irradiation the normal profile of ecdysteroid titers is restored, and ecdysteroid production from explanted ring glands is elevated.

(Sehnal and Bryant, 1993)

Larval life prolonged by up to 14 days. Overgrown larvae show bloating and an increase in water content.

(Zitnan et al., 1993)

Clonal analysis shows small clones for dlg1 can produce cuticle demonstrating that surrounding wild type tissue can partially rescue the defect in differentiation.

(Woods and Bryant, 1991)

Homozygotes fail to pupariate at 25^oC and die as very bloated larvae with some partially tanned cuticle. The larval brain show extensive overgrowth of the cerebral hemispheres. Irradiation of larvae results in 100% rescue of the pupariation delay.

(Poodry and Woods, 1990)

Hemizygous larvae have abnormal wing discs; the wing discs are smaller than normal and have an abnormal morphology up to the time of pupariation in normal larvae. Hemizygous larvae fail to pupariate at 25^oC, and have an extended third larval instar period compared to wild-type that lasts up to about 15 days after egg laying (AEL). During this time the wing discs overgrow, and by 11 days AEL begin to fuse with the haltere and third leg discs. The optic lobes of the brain also become greatly enlarged, and fusion occurs between the first and second leg discs and the ventral ganglion. All the imaginal discs appear to be affected in a similar manner, but fusion only occurs between discs that are close together. The larvae take on a swollen, bloated appearance during the extended third larval instar period. About 15 days AEL they form a "pseudopupa" with some tanning of the larval cuticle.

(Woods and Bryant, 1989)

External Data

Linkouts

Interactions

Show genetic interaction network for Enhancers & Suppressors

Phenotypic Class

Suppressed by

Statement

Reference

dlg1⁷ has abnormal neuroanatomy phenotype, suppressible by par-1^Δ-16/par-1[+]

(Zhang et al., 2007)

dlg1⁷ has neoplasia phenotype, suppressible by Rnor\Dlg3^UAS.cTa/Scer\GAL4^da.G32

(Thomas et al., 1997)

dlg1⁷ has neoplasia phenotype, suppressible by Scer\GAL4^elav.PLu/Rnor\Dlg1^UAS.cTa

(Thomas et al., 1997)

dlg1⁷ has neoplasia phenotype, suppressible by Rnor\Dlg3^UAS.cTa/Scer\GAL4^elav.PLu

(Thomas et al., 1997)

dlg1⁷ has flightless phenotype, suppressible by Rnor\Dlg3^UAS.cTa/Scer\GAL4^da.G32/Scer\GAL4^elav.PLu

(Thomas et al., 1997)

dlg1⁷ has neoplasia phenotype, suppressible by Scer\GAL4^da.G32/Rnor\Dlg1^UAS.cTa

(Thomas et al., 1997)

Enhancer of

Statement

Reference

dlg1[+]/dlg1⁷ is an enhancer of abnormal neuroanatomy phenotype of Scer\GAL4^Mhc.PW, par-1^UAS.cSa

(Zhang et al., 2007)

Suppressor of

Statement

Reference

dlg1⁷ is a suppressor of abnormal neuroanatomy phenotype of sei²

(Lee and Wu, 2010)

NOT Suppressor of

Statement

Reference

dlg1⁷ is a non-suppressor of abnormal neuroanatomy phenotype of slo¹

(Lee and Wu, 2010)

Phenotype Manifest In

Suppressed by

Statement

Reference

dlg1⁷ has NMJ bouton phenotype, suppressible by par-1^Δ-16/par-1[+]

(Zhang et al., 2007)

dlg1⁷ has imaginal disc phenotype, suppressible by Scer\GAL4^da.G32/Rnor\Dlg1^UAS.cTa

(Thomas et al., 1997)

dlg1⁷ has imaginal disc phenotype, suppressible by Rnor\Dlg3^UAS.cTa/Scer\GAL4^da.G32

(Thomas et al., 1997)

NOT suppressed by

Statement

Reference

dlg1⁷ has bouton phenotype, non-suppressible by Scer\GAL4^da.G32/Rnor\Dlg1^UAS.cTa

(Thomas et al., 1997)

dlg1⁷ has bouton phenotype, non-suppressible by Rnor\Dlg3^UAS.cTa/Scer\GAL4^da.G32

(Thomas et al., 1997)

Enhancer of

Statement

Reference

dlg1[+]/dlg1⁷ is an enhancer of NMJ bouton phenotype of par-1^UAS.cSa

(Zhang et al., 2007)

Suppressor of

Statement

Reference

dlg1⁷ is a suppressor of NMJ bouton | increased number phenotype of slo¹

(Lee and Wu, 2010)

dlg1⁷ is a suppressor of neuromuscular junction phenotype of slo¹

(Lee and Wu, 2010)

dlg1⁷ is a suppressor of NMJ bouton | increased number phenotype of sei²

(Lee and Wu, 2010)

dlg1⁷ is a suppressor of neuromuscular junction phenotype of sei²

(Lee and Wu, 2010)

NOT Suppressor of

Statement

Reference

dlg1⁷ is a non-suppressor of subsynaptic reticulum | ectopic phenotype of Scer\GAL4^C57, Syx18^UAS.cGa

(Gorczyca et al., 2007)

Additional Comments

Genetic Interactions

Statement

Reference

dlg1⁷/sei² mutants exhibit reduced levels of type B and type M satellites, close to wild-type levels, compared to sei² single mutants. These reduction correlates with reduced levels of mature boutons and with simpler branching patterns.

dlg1⁷/slo¹ mutants exhibit reduced levels of type B and type M satellites, close to wild-type levels, compared to slo¹ single mutants. This reduction correlates with reduced levels of mature boutons and with simpler branching patterns.

(Lee and Wu, 2010)

The ectopic subsynaptic reticulum-like structures seen in muscles expressing Syx18^Scer\UAS.cGa under the control of Scer\GAL4^C57 are not suppressed by dlg1⁷.

(Gorczyca et al., 2007)

dlg1⁷/+ enhances the reduction in the number boutons at the neuromuscular junction which is seen in animals expressing par-1^Scer\UAS.cSa under the control of Scer\GAL4^Mhc.PW.

par-1^Δ-16/+ partially suppresses the decrease in the number of boutons at the neuromuscular junction which is seen in dlg1⁷ homozygotes.

(Zhang et al., 2007)

The rescue of the dlg1⁷ neuromuscular junction defects by dlg1^{S48A.Scer\UAS.T:Avic\GFP} expressed under the control of Scer\GAL4^unspecified is unaltered by expression of CaMKII^{T287D.Scer\UAS} in the postsynaptic muscles.

(Koh et al., 1999)

The increased number of active zones is also rescued if Rnor\SAP97^Scer\UAS.cTa is targeted to both pre- and postsynaptic cells using Scer\GAL4^unspecified.

(Thomas et al., 1997)

Xenogenetic Interactions

Statement

Reference

The imaginal disc and brain tumour phenotypes of hemizygous males is partially rescued by Rnor\SAP97^Scer\UAS.cTa or Rnor\SAP102^Scer\UAS.cTa expressed using Scer\GAL4^da.G32, resulting in viable adults in some cases. These flies are flightless. Some of the flies rescued by Rnor\SAP97^Scer\UAS.cTa expressed using Scer\GAL4^da.G32 show patches of tumour-like outgrowth, particularly on the legs and wings. There is an 80% reduction in the number of viable dlg1⁷ males rescued by Rnor\SAP102^Scer\UAS.cTa expressed using Scer\GAL4^da.G32 if the flies are also heterozygous for Df(3L)H99, and all surviving flies have tumours. The neuromuscular junction presynaptic phenotype of hemizygous males is not rescued by Rnor\SAP97^Scer\UAS.cTa or Rnor\SAP102^Scer\UAS.cTa expressed using Scer\GAL4^da.G32, although the bouton structure does appear normal when Rnor\SAP97^Scer\UAS.cTa or Rnor\SAP102^Scer\UAS.cTa are expressed using Scer\GAL4^elav.PLu. The tumour phenotype of hemizygous males is not rescued by Rnor\SAP97^Scer\UAS.cTa or Rnor\SAP102^Scer\UAS.cTa expressed using Scer\GAL4^elav.PLu. Hemizygous males rescued by Rnor\SAP102^Scer\UAS.cTa expressed using Scer\GAL4^da.G32 together with Scer\GAL4^elav.PLu can fly.

(Thomas et al., 1997)

Complementation and Rescue Data

Partially complements

dlg1¹²

(Woods et al., 1996)

Fails to complement

dlg1¹⁸

(Goode and Perrimon, 1997)

dlg1¹⁴

(Goode and Perrimon, 1997)

dlg1¹³

(Goode and Perrimon, 1997)

dlg1⁶

(Goode and Perrimon, 1997)

dlg1⁵

(Goode and Perrimon, 1997)

dlg1¹⁸

(Woods et al., 1996)

dlg1¹⁵

(Woods et al., 1996)

dlg1¹⁴

(Woods et al., 1996)

dlg1⁶

(Woods et al., 1996)

Rescued by

dlg1⁷ is rescued by Scer\GAL4^Mhc.PW/dlg1^WT.UAS.GFP

(Zhang et al., 2007)

dlg1⁷ is rescued by Scer\GAL4^Mhc.PW/dlg1^SA.UAS.GFP

(Zhang et al., 2007)

dlg1⁷ is rescued by dlg1^{S48A.UAS.EGFP}/Scer\GAL4^unspecified

(Koh et al., 1999)

dlg1⁷ is rescued by Scer\GAL4^32B/dlg1^UAS.cBa

(Woods et al., 1996)

Partially rescued by

dlg1⁷ is partially rescued by Scer\GAL4^unspecified/dlg1^UAS.cBa

(Thomas et al., 1997)

Not rescued by

dlg1⁷ is not rescued by Scer\GAL4^Mhc.PW/dlg1^SD.UAS.GFP

(Zhang et al., 2007)

Comments

Scer\GAL4^32B mediated expression of dlg1^Scer\UAS.cBa rescues lethality to adulthood.

(Woods et al., 1996)

Images (0)

Mutant

Wild-type

Stocks (1)

Bloomington

90948

w^* dlg1⁷/FM7a/Dp(1;Y)y⁺

Notes on Origin

Discoverer

Comments

Class III mutation.

(Woods et al., 1996)

External Crossreferences and Linkouts ( 0 )

Synonyms and Secondary IDs (13)

Reported As

Symbol Synonym

XI-2

(Abbott and Schenkel, 1992, Woods and Bryant, 1989)

dlg-1^XI-2

(Thomas et al., 1997)

dlg1⁷

dlg^X1-2

(Wang et al., 2017, Lee and Wu, 2010, Kohsaka et al., 2007, Zhang et al., 2007, Caruana, 2002, Koh et al., 1999, Gundelfinger et al., 1998, Tejedor et al., 1997, Thomas et al., 1997)

dlg^X12

(Goode and Perrimon, 1997)

dlg^XI-12

(Gorczyca et al., 2007)

dlg^XI-2

(Bertin et al., 2022, Mendoza-Topaz et al., 2008, Gorczyca et al., 2007, Bachmann et al., 2004, Mendoza et al., 2003, Koh et al., 2002, Sone et al., 2000, Thomas et al., 2000, Woods et al., 1996, Woods and Bryant, 1991)

dlg^Xl-2

(Moyer and Jacobs, 2008)

dlg^x-1

(Wolfgang et al., 2004)

l(1)d.lg-1^XI-2

(Poodry and Woods, 1990, Gateff and Mechler, 1989)

l(1)d.lg-1^xi-2

(Zitnan et al., 1993)

l(1)d.lg.-1

l(1)dlg^X1-2

(Hanratty and Dearolf, 1993)

Name Synonyms

Secondary FlyBase IDs

References (33)

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