FlyBase Allele Report: Dmel\dlg1[14]

General Information

Symbol

Dmel\dlg1¹⁴

Species

D. melanogaster

Name

FlyBase ID

FBal0002683

Feature type

allele

Associated gene

Dmel\dlg1

Associated Insertion(s)

Carried in Construct

Also Known As

dlg^m52, dlg1^m52

Key Links

Genomic Maps

JBrowse

Allele class

loss of function allele

amorphic allele - genetic evidence

Mutagen

ethyl nitrosourea

Nature of the Allele

Allele class

amorphic allele - genetic evidence

(Lahey et al., 1994, Woods and Bryant, 1991)

loss of function allele

(Siegrist and Doe, 2005, Goode and Perrimon, 1997, Hough et al., 1997, Guan et al., 1996, Woods et al., 1996)

Mutagen

ethyl nitrosourea

(Woods and Bryant, 1989)

Progenitor genotype

Cytology

Description

The splice-site mutation of the dlg1 allele produces an unstable protein.

(Siegrist and Doe, 2005)

Splicing defect reveals a stop codon in intron 5 resulting in a truncated protein containing PDZ1, PDZ2 and the beginning of PDZ3.

(Tejedor et al., 1997)

Nucleotide substitution: G?A. Transition is at the splice donor for intron 5, resulting in stop codon near the beginning of PDZ/DHR3.

(Woods et al., 1996)

Mutations Mapped to the Genome

Curation Data

Type

Location

Additional Notes

References

point_mutation

X:11,397,913..11,397,913 [+]

Nucleotide change:

G11397913A

Reported nucleotide change:

G?A

Comment:

G to A transition at the splice donor for intron five that results in a stop codon near the beginning of the PDZ/DHR3 domain and a severely 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 ( 1 )

Disease

Evidence

References

model of cancer

CEA with Ras85D^V12.UAS

(Kakemura and Igaki, 2024, Pagliarini and Xu, 2003)

CEA

(Ohsawa et al., 2011)

model of carcinoma

CEA with Ras85D^V12.UAS

(Ito and Igaki, 2021, Igaki et al., 2006)

CEA

(Bilder et al., 2000)

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 cell polarity | somatic clone

(Igaki et al., 2006)

abnormal mitotic cell cycle | P-stage

(Bosveld et al., 2016)

abnormal neuroanatomy

(Budnik et al., 1996)

abnormal neuroanatomy | third instar larval stage (with Df(1)N71)

(Karunanithi et al., 2002)

abnormal neurophysiology

(Budnik et al., 1996)

abnormal neurophysiology | third instar larval stage (with Df(1)N71)

(Karunanithi et al., 2002)

hyperplasia

(Woods et al., 1997)

lethal | recessive

(Goode and Perrimon, 1997, Woods and Bryant, 1989)

lethal - all die before end of larval stage | recessive

(Thomas et al., 1997, Woods et al., 1996)

lethal - all die before end of pupal stage | recessive

(Lahey et al., 1994)

neoplasia | recessive

(Woodhouse et al., 1998)

some die during larval stage | recessive

(Thomas et al., 1997, Woods et al., 1996)

some die during pupal stage | recessive

(Lahey et al., 1994)

Phenotype Manifest In

adherens junction

(Bilder et al., 2003)

adherens junction | ectopic

(Woods et al., 1996)

brain | third instar larval stage (with Df(1)N71)

(Karunanithi et al., 2002)

centrosome | P-stage

(Bosveld et al., 2016)

egg chamber | somatic clone

(Abdelilah-Seyfried et al., 2003)

embryonic/first instar larval cuticle

(Blankenship et al., 2007)

embryonic epidermis | germline clone

(Woods and Bryant, 1991)

embryonic neuroblast

(Albertson and Doe, 2003)

epithelial cell | germline clone

(Peng et al., 2000)

epithelial cell | P-stage

(Bosveld et al., 2016)

eye-antennal disc

(Igaki et al., 2006)

follicle cell | cell autonomous | somatic clone

(Abdelilah-Seyfried et al., 2003)

follicle cell | germline clone

(Goode and Perrimon, 1997)

follicle cell | somatic clone

(Bilder et al., 2000, Goode and Perrimon, 1997)

germline cell | germline clone

(Goode and Perrimon, 1997)

imaginal disc

(Hough et al., 1997, Woods et al., 1996)

imaginal disc & epithelial cell & plasma membrane | somatic clone

(Lee et al., 2003)

imaginal disc & epithelial cell & septate junction | somatic clone

(Lee et al., 2003)

imaginal disc & septate junction

(Hough et al., 1997)

imaginal disc | third instar larval stage (with Df(1)N71)

(Karunanithi et al., 2002)

neuroblast | embryonic stage | germline clone

(Peng et al., 2000)

oocyte associated follicular epithelium | somatic clone

(Tian et al., 2023)

pleated septate junction

(Bilder et al., 2003)

postsynaptic membrane

(Budnik et al., 1996)

presumptive embryonic/larval nervous system | germline clone

(Woods and Bryant, 1991)

septate junction

(Woods et al., 1996)

subsynaptic reticulum | third instar larval stage

(Kumar et al., 2009)

synapse | third instar larval stage (with Df(1)N71)

(Karunanithi et al., 2002)

synaptic vesicle (with Df(1)N71)

(Karunanithi et al., 2002)

type I bouton | third instar larval stage (with Df(1)N71)

(Karunanithi et al., 2002)

Detailed Description

Statement

Reference

Eye/antennal disc clones both expressing Ras85D^V12.UAS under the control of Scer\GAL4^Act5C.PI and homozygous for dlg1¹⁴ form tumors.

(Cong et al., 2021)

dlg1¹⁴ significantly reduces centrosome recoil upon microtubule ablation (mean centrosome velocity relative to microtubule ablation site) compared to wild type.

(Bosveld et al., 2016)

Mutant third instar neuromuscular junctions show highly reduced subsynaptic reticulum.

(Kumar et al., 2009)

Mutant embryos produce a continuous, malformed cuticle.

(Blankenship et al., 2007)

dlg1¹⁴ mutant clones in cephalic complexes (including the eye-antennal discs) exhibit defects in cell polarity.

(Igaki et al., 2006)

dlg1¹⁴ mutant clones in the follicle cells become invasive about half the time - streams of cells are found to break out of the follicular epithelium at random points and to cross the germ cell poper, predominantly along the anterior-posterior axis of the egg chamber, but also in diverging directions relative to the position of the oocyte.

(Abdelilah-Seyfried et al., 2003)

Neuroblasts in homozygous stage 15 embryos (lacking zygotic dlg1 function) show defects in division; 80% undergo normal division, while 20% undergo a symmetrical division. Neuroblasts in stage 15 embryos derived from germline clones (lacking both maternal and zygotic dlg1 function) show defects in division; 68% undergo normal division, 22% undergo a symmetrical division and 10% undergo an inverted asymmetrical division.

(Albertson and Doe, 2003)

In stage 15 embryos lacking both maternal and zygotic dlg1 function the loosely adherent and rounded mutant epidermal cells reassociate to form coherent strips of cells that are highly polarised. Adherens junctions (which are mislocalised in mid-embryogenesis) become restricted to the junction of apical and basolateral surfaces, similar to wild-type epithelia. The pleated septate junction is not formed.

(Bilder et al., 2003)

dlg1¹⁴ mutant clones exhibit malformed plasma membranes disrupted into vesicles along with disrupted septate junctions.

(Lee et al., 2003)

dlg1¹⁴/Df(1)N71 wandering third instar larvae have large tumours on the brain and imaginal discs. The type 1 boutons of dlg1¹⁴/Df(1)N71 third instar larvae have larger synaptic vesicles and a larger synaptic area than in wild-type larvae. Quantal size is larger in the dlg1¹⁴ boutons, an increase that correlates well with the increase in vesicle volume, but not with that of synaptic area. Quantal variance is not significantly different from wild type.

(Karunanithi et al., 2002)

Follicle cell clones homozygous for dlg1¹⁴ show defects in morphology.

(Bilder et al., 2000)

Embryos derived from maternal homozygous germline clones show an early loss of embryonic epithelial apical/basal polarity and neuroblast defects.

(Peng et al., 2000)

The median survival of adult hosts transplanted with hemizygous dlg1¹⁴ brain fragments is reduced compared to adult hosts transplanted with wild-type brain fragments. Cells from transplanted hemizygous brain fragments form at least one secondary tumour in the wild-type host in 22% of cases. Imaginal discs from hemizygous dlg1¹⁴ larvae form large primary tumours but no detectable secondary tumours after transplantation into wild-type adult hosts.

(Woodhouse et al., 1998)

Follicle cells have an invasive phenotype, intermingling with germ cells in the egg chamber in females with homozygous dlg1¹⁴ clones in both the germ cells and follicle cells. Females with homozygous clones in the germ cells alone occasionally have misshaped germ cells but show no other defects. Females with homozygous clones in the follicle cells alone have an overaccumulation of follicle cells at the anterior and posterior poles of the egg chamber, but these follicle cells invade germ tissue only rarely.

(Goode and Perrimon, 1997)

Imaginal discs are composed of a dense mass of multilayered, noncolumnar epithelial cells that lack septate junctions and apicobasal polarity. Imaginal discs are also overgrown. These phenotypes can be rescued by Scer\GAL4^69B-mediated expression of dlg1^{Δt40.Scer\UAS.T:Zzzz\FLAG}, dlg1^{ΔGUK.Scer\UAS.T:Zzzz\FLAG} or dlg1^{ΔPDZ1.Scer\UAS.T:Zzzz\FLAG}.

(Hough et al., 1997)

Mutant shows no change in glutamate receptor localization.

(Petersen et al., 1997)

Homozygotes die as late third instar larvae.

(Thomas et al., 1997)

Neoplastic overgrowth mutant. Imaginal disc tissue shows abnormal distribution of apico-lateral cell junctional markers.

(Woods et al., 1997)

Presynaptic morphology is normal except for a small but significant reduction in vesicle density. Structural defects in the subsynaptic reticulum (SSR), it appears to be underdeveloped. Synaptic transmission is altered; increase in excitatory junctional currents (EJC) amplitude (not due to changes in passive properties of the muscle membrane but due to presynaptic defects causing increased neurotransmitter release).

(Budnik et al., 1996)

There are no abnormalities in the pathways axons follow, the growth cone morphology, or the time at which the growth cones reach their target and differentiate into boutons on muscles 6, 7, 12 and 13 in hemizygotes.

(Guan et al., 1996)

Homozygous larvae exhibit overgrown imaginal discs. Imaginal disc cells lack apicobasal polarity and septate junctions, adherens junctions are still present at various ectopic positions on the cell membrane. Salivary gland cells still have obvious apicobasal polarity, but the septate junctions are reduced to a small fraction. The basolateral membrane is highly disrupted.

(Woods et al., 1996)

Lethality occurs during metamorphosis with neoplastic growth in imaginal discs and CNS.

(Lahey et al., 1994)

Mitotic recombination in the female germline produces embryos with abnormal segmentation in the epidermis and nervous system, but which can make recognized cuticular derivatives.

(Woods and Bryant, 1991)

dlg1⁴/dlg1² lethal at 18^oC

External Data

Linkouts

Interactions

Show genetic interaction network for Enhancers & Suppressors

Phenotypic Class

Enhanced by

Statement

Reference

dlg1¹⁴ has lethal | larval stage | recessive phenotype, enhanceable by Sh⁷/Sh⁷

(Thomas et al., 1997)

Suppressed by

Statement

Reference

Ras85D^V12.UAS, Scer\GAL4^Act5C.PI, dlg1¹⁴ has neoplasia | somatic clone | larval stage phenotype, suppressible by Rheb^HMS00923, Scer\GAL4^Act5C.PI

(Cong et al., 2021)

Ras85D^V12.UAS, Scer\GAL4^Act.PU, dlg1¹⁴ has neoplasia | somatic clone | larval stage phenotype, suppressible | partially by pnt^P1.UAS, Scer\GAL4^Act.PU

(Ito and Igaki, 2021)

Enhancer of

Statement

Reference

dlg1¹⁴/dlg1¹⁴ is an enhancer of neoplasia | larval stage | somatic clone phenotype of Ras85D^V12.UAS, Scer\GAL4^Act.PU

(Ito and Igaki, 2021)

dlg1[+]/dlg1¹⁴ is an enhancer of visible phenotype of Scer\GAL4^GMR.PF, crb^intra.UAS

(Tanentzapf and Tepass, 2003)

dlg1¹⁴ is an enhancer of visible phenotype of Scer\GAL4^en-e16E, arm^UAS.cWa

(Greaves et al., 1999)

Suppressor of

Statement

Reference

dlg1¹⁴ is a suppressor of visible phenotype of Scer\GAL4^en-e16E, shg^{i.UAS.Tag:SS(aos),Tag:MYC}

(Greaves et al., 1999)

Other

Statement

Reference

Ras85D^V12.UAS, Scer\GAL4^Act5C.PI, dlg1¹⁴ has neoplasia | somatic clone | larval stage phenotype

(Cong et al., 2021)

Ras85D^V12.UAS, dlg1¹⁴ has neoplasia | somatic clone phenotype

(Igaki et al., 2006)

Ras85D^V12.UAS, Scer\GAL4^Act5C.PI, dlg1¹⁴ has neoplasia phenotype

(Igaki et al., 2006)

Phenotype Manifest In

Suppressed by

Statement

Reference

Ras85D^V12.UAS, Scer\GAL4^Act5C.PI, dlg1¹⁴ has eye-antennal disc | somatic clone | larval stage phenotype, suppressible by Rheb^HMS00923, Scer\GAL4^Act5C.PI

(Cong et al., 2021)

Ras85D^V12.UAS, Scer\GAL4^Act.PU, dlg1¹⁴ has eye-antennal disc | somatic clone phenotype, suppressible | partially by pnt^P1.UAS, Scer\GAL4^Act.PU

(Ito and Igaki, 2021)

dlg1¹⁴ has follicle cell | somatic clone phenotype, suppressible by baz^EH171

(Abdelilah-Seyfried et al., 2003)

Enhancer of

Statement

Reference

dlg1¹⁴/dlg1¹⁴ is an enhancer of eye-antennal disc | somatic clone phenotype of Ras85D^V12.UAS, Scer\GAL4^Act.PU

(Ito and Igaki, 2021)

dlg1[+]/dlg1¹⁴ is an enhancer of eye phenotype of Scer\GAL4^GMR.PF, crb^intra.UAS

(Tanentzapf and Tepass, 2003)

dlg1¹⁴ is an enhancer of wing phenotype of Scer\GAL4^en-e16E, arm^UAS.cWa

(Greaves et al., 1999)

NOT Enhancer of

Statement

Reference

dlg1[+]/dlg1¹⁴ is a non-enhancer of ommatidium phenotype of Vang^stbm-153

(Courbard et al., 2009)

Suppressor of

Statement

Reference

dlg1¹⁴ is a suppressor of embryonic/first instar larval cuticle phenotype of Exo84^Z4840/Df(3R)Espl3

(Blankenship et al., 2007)

dlg1[+]/dlg1¹⁴ is a suppressor of embryonic/first instar larval cuticle phenotype of crb^11A22

(Tanentzapf and Tepass, 2003)

dlg1¹⁴/dlg1¹⁴ is a suppressor of embryonic/first instar larval cuticle phenotype of crb^11A22

(Tanentzapf and Tepass, 2003)

dlg1¹⁴ is a suppressor of wing phenotype of Scer\GAL4^en-e16E, shg^{i.UAS.Tag:SS(aos),Tag:MYC}

(Greaves et al., 1999)

NOT Suppressor of

Statement

Reference

dlg1[+]/dlg1¹⁴ is a non-suppressor of ommatidium phenotype of Vang^stbm-153

(Courbard et al., 2009)

dlg1¹⁴ is a non-suppressor of embryonic/first instar larval cuticle phenotype of yrt⁷⁵

(Laprise et al., 2006)

Other

Statement

Reference

Ras85D^V12.UAS, Scer\GAL4^Act5C.PI, dlg1¹⁴ has eye-antennal disc | somatic clone | larval stage phenotype

(Cong et al., 2021)

Scer\GAL4^Mef2.PR, Synd^UAS.cKa, dlg1¹⁴ has subsynaptic reticulum | third instar larval stage phenotype

(Kumar et al., 2009)

Additional Comments

Genetic Interactions

Statement

Reference

Heterozygosity for dlg1¹⁴ has no effect on the frequency of ommatidia that show planar cell polarity defects in Vang^stbm-153 homozygotes.

(Courbard et al., 2009)

Scer\GAL4^Mef2.PR-mediated expression of Synd^Scer\UAS.cKa can induce postsynaptic membrane expansions in dlg1¹⁴ mutants that show highly reduced subsynaptic reticulum.

(Kumar et al., 2009)

The cuticle defects seen at 25[o]C in embryos derived from exo84^onr/Df(3R)Espl3 females mated to exo84^onr heterozygous males are suppressed by dlg1¹⁴.

(Blankenship et al., 2007)

dlg1¹⁴ mutant clones expressing Ras85D^V12.Scer\UAS under the control of Scer\GAL4^Act5C.PI exhibit invasive tumours.

(Igaki et al., 2006)

The yrt⁷⁵ cuticle phenotype is not modified in yrt⁷⁵, dlg1¹⁴ double zygotic mutant embryos.

(Laprise et al., 2006)

baz^EH171, dlg1¹⁴ double mutant clones in the follicle cells exhibit a rough germline boundary, but do not exhibit any invasive properties.

(Abdelilah-Seyfried et al., 2003)

dlg1¹⁴ ; l(2)gl^unspecified/+ neuroblasts show defects in division; 59% undergo normal division, 26% undergo a symmetrical division and 15% undergo an inverted asymmetrical division. dlg1¹⁴ ; scrib¹/+ neuroblasts show defects in division; 52% undergo normal division, 32% undergo a symmetrical division and 16% undergo an inverted asymmetrical division. dlg1¹⁴ ; l(2)gl^unspecified/+ ; scrib¹/+ neuroblasts show defects in division; 56% undergo normal division, 22% undergo a symmetrical division and 22% undergo an inverted asymmetrical division.

(Albertson and Doe, 2003)

dlg1¹⁴ sdt^unspecified embryos (which lack both maternal and zygotic dlg1 and sdt function) have cuticle phenotypes which are indistinguishable from dlg1¹⁴ embryos lacking maternal and zygotic dlg1 function. At mid-embryogenesis, adherens junctions are mis-localised to basolateral surfaces. dlg1¹⁴ sdt^unspecified zygotically mutant embryos produce continuous patches of cuticle. dlg1¹⁴ baz⁴ embryos (which lack both maternal and zygotic dlg1 and baz function) have cuticle phenotypes which are indistinguishable from baz⁴ embryos lacking maternal and zygotic baz function; the embryos show a severe loss of post-gastrulation adherens junctions and fail to produce cuticle.

(Bilder et al., 2003)

Marked clones in the eye disc expressing Ras85D^V12.Scer\UAS under the control of Scer\GAL4^Act5C.PI and which are also homozygous for dlg1¹⁴ show metastatic behaviour.

(Pagliarini and Xu, 2003)

Enhances the wing phenotype caused by expression of arm^Scer\UAS.cWa under the control of Scer\GAL4^en-e16E. Suppresses the wing phenotype caused by expression of argos::shg^{i.Scer\UAS.T:Hsap\MYC} under the control of Scer\GAL4^en-e16E.

(Greaves et al., 1999)

dlg1¹⁴ Sh⁷ double homozygotes die as first or second instar larvae.

(Thomas et al., 1997)

Xenogenetic Interactions

Statement

Reference

Complementation and Rescue Data

Fails to complement

Rescued by

dlg1¹⁴ is rescued by Scer\GAL4^Act5C.PU/dlg1^UAS.Tag:HA

(Sharp et al., 2021)

dlg1¹⁴ is rescued by dlg1^{Δt40.UAS.Tag:FLAG}/Scer\GAL4^69B

(Hough et al., 1997)

dlg1¹⁴ is rescued by dlg1^{ΔGUK.UAS.Tag:FLAG}/Scer\GAL4^69B

(Hough et al., 1997)

dlg1¹⁴ is rescued by dlg1^UAS.cBa/Scer\GAL4^BG487

(Tejedor et al., 1997)

dlg1¹⁴ is rescued by Scer\GAL4^sca.PC/dlg1^UAS.cBa

(Budnik et al., 1996)

dlg1¹⁴ is rescued by Scer\GAL4^BG380/dlg1^UAS.cBa

(Budnik et al., 1996)

dlg1¹⁴ is rescued by Scer\GAL4^32B/dlg1^UAS.cBa

(Woods et al., 1996)

Partially rescued by

dlg1¹⁴/Df(1)N71 is partially rescued by dlg1^UAS.cBa/Scer\GAL4^BG487

(Karunanithi et al., 2002)

dlg1¹⁴/Df(1)N71 is partially rescued by Scer\GAL4^BG380/dlg1^UAS.cBa

(Karunanithi et al., 2002)

dlg1¹⁴ is partially rescued by dlg1^{ΔSH3.UAS.Tag:FLAG}/Scer\GAL4^69B

(Hough et al., 1997)

dlg1¹⁴ is partially rescued by dlg1^{ΔPDZ2:3.UAS.Tag:FLAG}/Scer\GAL4^69B

(Hough et al., 1997)

dlg1¹⁴ is partially rescued by dlg1^{ΔPDZ1.UAS.Tag:FLAG}/Scer\GAL4^69B

(Hough et al., 1997)

dlg1¹⁴ is partially rescued by dlg1^{ΔPDZ2.UAS.Tag:FLAG}/Scer\GAL4^69B

(Hough et al., 1997)

dlg1¹⁴ is partially rescued by dlg1^UAS.cBa/Scer\GAL4^BG487

(Budnik et al., 1996)

dlg1¹⁴ is partially rescued by dlg1^UAS.cBa/Scer\GAL4^C57

(Budnik et al., 1996)

Not rescued by

dlg1¹⁴ is not rescued by Scer\GAL4^Act5C.PU/dlg1^{2xNLS-A.UAS.Tag:HA}

(Sharp et al., 2021)

dlg1¹⁴ is not rescued by dlg1^{ΔN2:3.UAS.Tag:FLAG}/Scer\GAL4^69B

(Hough et al., 1997)

dlg1¹⁴ is not rescued by dlg1^{ΔC1:2.UAS.Tag:FLAG}/Scer\GAL4^69B

(Hough et al., 1997)

dlg1¹⁴ is not rescued by dlg1^{ΔHOOK.UAS.Tag:FLAG}/Scer\GAL4^69B

(Hough et al., 1997)

dlg1¹⁴ is not rescued by dlg1^{ΔPDZ1:2.UAS.Tag:FLAG}/Scer\GAL4^69B

(Hough et al., 1997)

Comments

Expression of dlg1^Scer\UAS.cBa, driven by either Scer\GAL4^BG380 or Scer\GAL4^BG487, rescues the neurological phenotype of dlg1¹⁴/Df(1)N71 mutants, leading to wild-type vesicle and quantal size. The synaptic area is reduced to a wild-type size in type 1s boutons, while in type 1b boutons, the rescued synaptic area is actually smaller than wild-type controls.

(Karunanithi et al., 2002)

Abnormal Sh clustering phenotype can be rescued by Scer\GAL4^BG487-mediated expression of dlg1^Scer\UAS.cBa.

(Tejedor et al., 1997)

Scer\GAL4^BG487 or Scer\GAL4^C57 mediated postsynaptic expression of dlg1^Scer\UAS.cBa partially rescues the SSR mutant phenotype at type I synapses, Scer\GAL4^sca.PC or Scer\GAL4^BG380 mediated presynaptic expression fully rescues.

(Budnik et al., 1996)

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

36283

w^* dlg1¹⁴ P{FRT(w^hs)}101/FM7a; PBac{PB}CG11583^c01124 P{neoFRT}80B/TM3, Sb¹

Notes on Origin

Discoverer

Voelker.

Comments

Class I mutation.

(Woods et al., 1996)

Clonal analysis indicates that dlg1 acts in both germ cells and follicle cells to block cellular invasion.

(Goode and Perrimon, 1997)

External Crossreferences and Linkouts ( 0 )

Synonyms and Secondary IDs (11)

Reported As

Symbol Synonym

Dlg^m52

(Tian et al., 2023)

dlg-m52

(Gerlach et al., 2022)

dlg1¹⁴

(Chen et al., 2018)

dlg1^m52

(Kakemura and Igaki, 2024, Donohoe et al., 2018, Garelli et al., 2012, Maiya et al., 2012)

dlg¹⁴

(Sizemore et al., 2023)

dlg^M52

(Bell et al., 2015, Tanentzapf and Tepass, 2003, Peng et al., 2000, Greaves et al., 1999)

dlg^m52

(Gerlach et al., 2022, Khoury and Bilder, 2022, Cong et al., 2021, Ito and Igaki, 2021, Sharp et al., 2021, Khoury and Bilder, 2020, Mishra-Gorur et al., 2019, Golub et al., 2017, Roubinet et al., 2017, Yamamoto et al., 2017, Bosveld et al., 2016, Kim et al., 2016, Roth et al., 2015, Izumi et al., 2012, Ohsawa et al., 2011, Courbard et al., 2009, Kumar et al., 2009, Denef et al., 2008, Blankenship et al., 2007, Igaki et al., 2006, Igaki et al., 2006, Laprise et al., 2006, Schulte et al., 2006, Siegrist and Doe, 2005, Bachmann et al., 2004, Szafranski and Goode, 2004, Abdelilah-Seyfried et al., 2003, Albertson and Doe, 2003, Lee et al., 2003, Mendoza et al., 2003, Pagliarini and Xu, 2003, Caruana, 2002, Karunanithi et al., 2002, Bilder et al., 2000, Ohshiro et al., 2000, Atwood et al., 1999, Koh et al., 1999, Woodhouse et al., 1998, Goode and Perrimon, 1997, Hough et al., 1997, Petersen et al., 1997, Tejedor et al., 1997, Thomas et al., 1997, Woods et al., 1997, Budnik et al., 1996, Guan et al., 1996, Woods et al., 1996, Lahey et al., 1994, Woods and Bryant, 1991)

dlgm⁵²

(Bilder et al., 2003)

l(1)M52

l(1)d.lg-1^m52

(Gateff and Mechler, 1989)

m52

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

Name Synonyms

Secondary FlyBase IDs

References (65)

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