FlyBase Allele Report: Dmel\DCTN1-p150[Gl-1]

General Information

Symbol

Dmel\DCTN1-p150^Gl-1

Species

D. melanogaster

Name

FlyBase ID

FBal0005065

Feature type

allele

Associated gene

Dmel\DCTN1-p150

Associated Insertion(s)

roo{}DCTN1-p150¹

Carried in Construct

Also Known As

Gl¹, Glued¹, Glu¹, Gl

Key Links

Allele class

amorphic allele - genetic evidence

Mutagen

heat

Nature of the Allele

Allele class

amorphic allele - genetic evidence

(Ghosh-Roy et al., 2004)

Mutagen

heat

(Plough and Ives, 1934)

Progenitor genotype

Associated Insertion(s)

roo{}DCTN1-p150¹

Cytology

Polytene chromosomes normal (Bridges).

Description

Insert stated as cause: undefined Insertion of a transposon into the 3' end of the gene, resulting in the production of an abnormal truncated transcript.

(Holzbaur et al., 1991)

Insertion of a roo element at the 3' end of the Gl gene.

(Swaroop et al., 1986)

Insertion of a 9kb roo element near the 3' end of the transcribed region, which results in a truncated transcript. The direction of transcription of the roo element is the same as the direction of Gl transcription.

(Swaroop et al., 1985)

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 ( 1 )

Disease

Interaction

References

exacerbates spinocerebellar ataxia type 5

modeled by Hsap\SPTBN2^{AM.UASp.Tag:MYC}

(Lorenzo et al., 2010)

modeled by β-Spec^GM.UAS

(Lorenzo et al., 2010)

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

Disease-implicated variant(s)

Phenotypic Data

Phenotypic Class

abnormal eye color | dominant

(Plough and Ives, 1934)

abnormal neuroanatomy

(Murphey et al., 1999)

abnormal neuroanatomy | adult stage | dominant

(Ma et al., 2009)

abnormal neuroanatomy | pupal stage

(Reddy et al., 1997)

abnormal neurophysiology

(Allen et al., 1999)

abnormal neurophysiology | adult stage | dominant

(Ma et al., 2009)

abnormal size | adult stage

(Fan and Ready, 1997)

decreased cell number | adult stage

(Fan and Ready, 1997)

fertile

lethal

(Swaroop et al., 1985)

lethal | recessive

(Holzbaur et al., 1991, Plough and Ives, 1934)

short lived

(Rawson et al., 2012)

viable

visible

(Fan and Ready, 1997)

visible | adult stage

(Lorenzo et al., 2010)

visible | dominant

(Ma et al., 2009, Iyadurai et al., 2008, Boylan and Hays, 2002, Boylan et al., 2000, McGrail et al., 1995, Harte and Kankel, 1982, Plough and Ives, 1934)

Phenotype Manifest In

adult optic lobe

(Harte and Kankel, 1982)

cone cell

(Fan and Ready, 1997)

eye

(Hain et al., 2014, Lorenzo et al., 2010, Ma et al., 2009, Iyadurai et al., 2008, Boylan et al., 2000, Mosley-Bishop et al., 1999, Fan and Ready, 1997, McGrail et al., 1995, Harte and Kankel, 1982, Plough and Ives, 1934)

eye photoreceptor cell

(Fan and Ready, 1997)

eye photoreceptor cell & microtubule

(Whited et al., 2004)

eye photoreceptor cell & nucleus

(Whited et al., 2004)

giant fiber neuron

(Ma et al., 2009, Allen et al., 1999)

giant fibers & synapse

(Allen et al., 1999)

Golgi apparatus

(Chang et al., 2013)

interommatidial bristle

(Fan and Ready, 1997, McGrail et al., 1995)

lipid droplet | maternal effect

(Gross et al., 2002)

macrochaeta

mesothoracic femoral chordotonal organ & axon

(Murphey et al., 1999)

metathoracic femoral chordotonal organ & axon

(Murphey et al., 1999)

mitochondrion

(Pilling et al., 2006)

motor neuron

(Reddy et al., 1997)

nervous system & thorax & pupa

(Reddy et al., 1997)

ommatidium

(Lorenzo et al., 2010, Ma et al., 2009, Boylan and Hays, 2002, Boylan et al., 2000, McGrail et al., 1995, Plough and Ives, 1934)

ommatidium | adult stage

(Fan and Ready, 1997)

photoreceptor neuron

(Mosley-Bishop et al., 1999)

pigment cell

(Plough and Ives, 1934)

primary pigment cell

(Fan and Ready, 1997)

prothoracic femoral chordotonal organ & axon

(Murphey et al., 1999)

rhabdomere

(Ma et al., 2009, Fan and Ready, 1997)

secondary pigment cell

(Fan and Ready, 1997)

sensillum trichodeum & leg & axon

(Murphey et al., 1999)

sensory neuron

(Reddy et al., 1997)

synapse

(Eaton et al., 2002)

tertiary pigment cell

(Fan and Ready, 1997)

Detailed Description

Statement

Reference

Gl¹/+ flies have small, rough eyes.

(Hain et al., 2014)

Homozygous single-cell DL1 olfactory projection neuron clones do not show obvious defects in axon elongation of dendrite branching.

(Sakuma et al., 2014)

Survival data from virgin females generated on standard laboratory food demonstrate that Gl¹ mutants have significant reduction in survival including changes in median and maximum lifespan compared with wild-type.

(Rawson et al., 2012)

The terminal cells in Gl¹ mutant trachea have thin cytoplasmic branches that lack air filling. Seamless tubes do not extend into these branches, although acetylated microtubules often do. Formation of filopodia at branch tips is disrupted and ectopic seamless tubes that are not air filled are detected near the nucleus. Discontinuous apical membrane fragments are found in terminal branches lacking seamless tubes and are associated with microtubule tracts.

(Schottenfeld-Roames and Ghabrial, 2012)

Gl¹ heterozygous flies exhibit a rough eye phenotype, with disordered ommatidia.

(Lorenzo et al., 2010)

Heterozygotes have roughened eyes which are smaller than normal. The ommatidia are disordered and irregularly shaped, and often have aberrant numbers of rhabdomeres.

8% of giant axon fibers lack the characteristic terminal bend in heterozygous adults.

Heterozygotes show electrophysiological defects in the giant fiber system; their response latency to brain stimulation is not significantly different from wild type, but they do not follow 1:1 on stimulation at a frequency of 250Hz as seen in wild-type flies.

(Ma et al., 2009)

Heterozygotes have a rough eye phenotype.

(Iyadurai et al., 2008, Boylan and Hays, 2002)

The motor axons of Gl¹/+ larvae show altered mitochondrial transport parameters compared to wild-type larvae. For anterograde mitochondria, the duty cycle shows a significant shift from pauses to forward runs and forward run velocity is increased. For retrograde mitochondria, duty cycles are not detectably affected, but there is a significant increase in forward run velocity.

(Pilling et al., 2006)

There is a significant reduction in the speed of mRNA transport in Gl¹ embryos. However, there is no change in the retention of injected mRNA at the apical cytoplasm following transport.

(Delanoue and Davis, 2005)

In the retinal photoreceptors of late third instar Gl¹/+ larvae, the region of the photoreceptor containing the nucleus often leaves the retina and travels through the optic stalk towards the brain. Both leading and trailing processes extend from these misplaced nuclei - in most cases both processes extend to the normal termini of the wild-type photoreceptor. Apical markers remain localised to the sites of processes remaining in the retina. These attachment sites have approximately normal spacing. However, apical-basal organisation of microtubules appears to be disrupted.

(Whited et al., 2004)

In Gl¹ embryos, the number of synaptic fingerprints (seen after synapses retract) at the synapse on muscles 6 and 7 is significantly increased (about 30% of synapses) compared to controls (6-7% of synapses), suggesting a reduction in synaptic stability at the neuromuscular junction.

(Eaton et al., 2002)

In embryos laid by Gl¹/+ females the force (applied with optical tweezers) required to stall plus end travel of lipid droplets is significantly less than for wild-type (WT) embryos. For plus end travel, lipid droplets in these mutant embryos also exhibit: an increase in the ratio of short runs to long runs (2.44+/-0.82 vs 1.05+/-0.22 in WT); an increase in pause frequency; and a slight increase in pause length. The minus end travel of lipid droplets in these mutants exhibits none of these differences with wild-type. However, average travel distance for both plus and minus end travel, is dramatically reduced.

(Gross et al., 2002)

Heterozygotes have a rough eye phenotype due to disruption of the organisation of the ommatidia.

(Boylan et al., 2000)

Heterozygotes show normal giant fiber morphology, though the physiology of the giant fibre is altered. The function of the GF-TTM synapse is altered in that repetitive stimulation leads to failures of response, at 250Hz. Average following frequency is 42.9%. Gl¹ compromises the chemical component of the GF-TTM synapse. There is a strong depression in the response of the TTM to stimulation of the GF at 200 Hz and 300 Hz.

(Allen et al., 1999)

Heterozygous larvae have no paralytic phenotypes.

(Martin et al., 1999)

In Gl¹ mutant eye discs the photoreceptor cell nuclei remain basal, rather than migrating apically as in wild-type.

(Mosley-Bishop et al., 1999)

In Gl¹/+ mutant flies there is no detectable difference from wild type until 30h APF. By 42h APF the differences are dramatic. The axons of the femoral chordotonal organ and tactile axons show abnormal terminal branching. The main bundle of femoral chordotonal organ axons is misplaced anteriorly and their collaterals are seldom detected. The main axon bundle appears scrambled. Similar phenotypes are seen in the tactile axons. Haltere axons and hair plate axons are unaffected. These phenotypes are similar to those caused by ctp^e73.

(Murphey et al., 1999)

Eyes are small and rough with few and irregularly positioned bristles. Ommatidial structure is severely disturbed, the number of photoreceptors is variable but usually less than normal, rhabdomeres are usually smaller than wild type. Mitosis is delayed in the second mitotic wave but the frequency of individual mitotic stages or spindle architecture is unchanged. Photoreceptor nuclei are distributed randomly throughout the eye disc, few occupy the normal apical region and many have fallen into the optic stalk. Defects in nuclear migration are due to defects in motor activity, not gross defects in the microtubule cytoskeleton. Cell fate determination of cells born in the second mitotic wave is disrupted. The number of cone cells and primary pigment cells per ommatidium is reduced, the number and organisation of secondary and tertiary pigment cells is also abnormal. A broad band of cell death occurs behind the morphogenetic furrow. Rhabdomeres are malformed due to defect in the targeted delivery of the membrane vesicles that build the rhabdomeres.

(Fan and Ready, 1997)

Mutation disrupts the sensory axons in the pupal thoracic nervous system but does not alter the lay of nervous system innervated by chordotonal axons. Mutation disrupts the resistance reflex between the sensory neurons of the chordotonal organ and the tibial extensor motor neurons.

(Reddy et al., 1997)

Heterozygotes have a rough eye phenotype, with disorganised and misshapen ommatidia. The alignment of bristles in the eye is disrupted.

(McGrail et al., 1995)

Dominant mutation.

(Holzbaur et al., 1991)

Heterozygotes have smaller eyes than normal which are oblong in shape. There is a clear space around the edge of the eye (as in lz "Spectacled" mutants), the facets are rounded and the eye surface is smooth and shiny as though "Glued". The phenotype resembles gl mutants. Eye colour: slightly darker than wild type.

(Plough and Ives, 1934)

Gl¹/Df(3L)Gl2 lethal period: embryo/early first instar. Eyes rough, smaller, and oblong; facets rounded; surface smooth and shinylike gl. Bristles generally shortened slightly and straighter than normal. RK1.

External Data

Linkouts

Interactions

Show genetic interaction network for Enhancers & Suppressors

Phenotypic Class

Enhanced by

Statement

Reference

DCTN1-p150^Gl-1 has visible | adult stage phenotype, enhanceable by Hsap\SPTBN2^{AM.UASp.Tag:MYC}/Scer\GAL4^GMR.PF

(Lorenzo et al., 2010)

DCTN1-p150^Gl-1 has visible | adult stage phenotype, enhanceable by β-Spec^GM.UAS/Scer\GAL4^GMR.PF

(Lorenzo et al., 2010)

DCTN1-p150^Gl-1 has visible | dominant phenotype, enhanceable by Su(H)[+]/Su(H)^EG37

(Ma et al., 2009)

DCTN1-p150^Gl-1 has abnormal neurophysiology | adult stage | dominant phenotype, enhanceable by Su(H)[+]/Su(H)^EG37

(Ma et al., 2009)

DCTN1-p150^Gl-1 has visible | dominant phenotype, enhanceable by EG162[+]/EG162^EG162

(Ma et al., 2009)

DCTN1-p150^Gl-1 has abnormal neurophysiology | adult stage | dominant phenotype, enhanceable by EG162[+]/EG162^EG162

(Ma et al., 2009)

DCTN1-p150^Gl-1 has abnormal neuroanatomy | adult stage | dominant phenotype, enhanceable by EG7[+]/EG7^EG7

(Ma et al., 2009)

DCTN1-p150^Gl-1 has abnormal neurophysiology | adult stage | dominant phenotype, enhanceable by EG7[+]/EG7^EG7

(Ma et al., 2009)

DCTN1-p150^Gl-1 has abnormal neuroanatomy | adult stage | dominant phenotype, enhanceable by EG56^EG56/EG56[+]

(Ma et al., 2009)

DCTN1-p150^Gl-1 has abnormal neurophysiology | adult stage | dominant phenotype, enhanceable by EG56^EG56/EG56[+]

(Ma et al., 2009)

DCTN1-p150^Gl-1 has abnormal neuroanatomy | adult stage | dominant phenotype, enhanceable by EG79[+]/EG79^EG79

(Ma et al., 2009)

DCTN1-p150^Gl-1 has abnormal neurophysiology | adult stage | dominant phenotype, enhanceable by EG79[+]/EG79^EG79

(Ma et al., 2009)

DCTN1-p150^Gl-1 has abnormal neurophysiology | adult stage | dominant phenotype, enhanceable by EG28^EG28/EG28[+]

(Ma et al., 2009)

DCTN1-p150^Gl-1 has abnormal neurophysiology | adult stage | dominant phenotype, enhanceable by EG149^EG149/EG149[+]

(Ma et al., 2009)

DCTN1-p150^Gl-1 has abnormal neurophysiology | adult stage | dominant phenotype, enhanceable by EG165[+]/EG165^EG165

(Ma et al., 2009)

DCTN1-p150^Gl-1 has visible | dominant phenotype, enhanceable by S[+]/S^rK134

(Iyadurai et al., 2008)

DCTN1-p150^Gl-1 has visible | dominant phenotype, enhanceable by S[+]/S¹

(Iyadurai et al., 2008)

DCTN1-p150^Gl-1 has visible | dominant phenotype, enhanceable by Df(2L)S3/+

(Iyadurai et al., 2008)

DCTN1-p150^Gl-1, S[+]/S¹ has visible | dominant phenotype, enhanceable by Dhc64C[+]/Dhc64C^1-1

(Iyadurai et al., 2008)

DCTN1-p150^Gl-1 has visible | dominant phenotype, enhanceable by sw^Dic-2/sw[+]

(Boylan and Hays, 2002)

DCTN1-p150^Gl-1 has visible | dominant phenotype, enhanceable by sw¹/sw[+]

(Boylan and Hays, 2002)

DCTN1-p150^Gl-1 has visible | dominant phenotype, enhanceable by sw^Dic-3/sw[+]

(Boylan and Hays, 2002)

DCTN1-p150^Gl-1 has visible | dominant phenotype, enhanceable by sw[+]/sw^Dic-1

(Boylan and Hays, 2002)

DCTN1-p150^Gl-1 has visible | dominant phenotype, enhanceable by Dhc64C[+]/Dhc64C^6-8

(McGrail et al., 1995)

DCTN1-p150^Gl-1 has visible | dominant phenotype, enhanceable by Dhc64C[+]/Dhc64C^6-10

(McGrail et al., 1995)

NOT Enhanced by

Statement

Reference

DCTN1-p150^Gl-1 has abnormal neurophysiology | adult stage | dominant phenotype, non-enhanceable by Su(H)[+]/Su(H)¹

(Ma et al., 2009)

DCTN1-p150^Gl-1 has abnormal neuroanatomy | adult stage | dominant phenotype, non-enhanceable by Su(H)[+]/Su(H)¹

(Ma et al., 2009)

DCTN1-p150^Gl-1 has visible | dominant phenotype, non-enhanceable by Df(3L)10^H

(McGrail et al., 1995)

Suppressed by

Statement

Reference

DCTN1-p150^Gl-1 has visible | dominant phenotype, suppressible by SG13^SG13/SG13[+]

(Ma et al., 2009)

DCTN1-p150^Gl-1 has visible | dominant phenotype, suppressible by SG46[+]/SG46^SG46

(Ma et al., 2009)

DCTN1-p150^Gl-1 has visible | dominant phenotype, suppressible by Dhc64C^8-1

(Iyadurai et al., 2008)

DCTN1-p150^Gl-1 has visible | dominant phenotype, suppressible by Dhc64C^8-1/Dhc64C⁷⁷

(Iyadurai et al., 2008)

DCTN1-p150^Gl-1 has visible | dominant phenotype, suppressible by sw^+t11

(Boylan et al., 2000)

DCTN1-p150^Gl-1 has visible | dominant phenotype, suppressible by Dhc64C^6-6/Dhc64C[+]

(McGrail et al., 1995)

NOT suppressed by

Statement

Reference

DCTN1-p150^Gl-1, S[+]/S¹ has visible | dominant phenotype, non-suppressible by Dhc64C⁷⁷/Su(Gl)77[+]

(Iyadurai et al., 2008)

DCTN1-p150^Gl-1, S[+]/S¹ has visible | dominant phenotype, non-suppressible by Dhc64C[+]/Dhc64C^8-1

(Iyadurai et al., 2008)

DCTN1-p150^Gl-1, S[+]/S¹ has visible | dominant phenotype, non-suppressible by Dhc64C^8-1/Dhc64C⁷⁷

(Iyadurai et al., 2008)

DCTN1-p150^Gl-1 has visible | dominant phenotype, non-suppressible by Df(3L)10^H

(McGrail et al., 1995)

Enhancer of

Statement

Reference

DCTN1-p150^Gl-1 is an enhancer | somatic clone of abnormal neuroanatomy | somatic clone phenotype of Strip^dogi

(Sakuma et al., 2014)

DCTN1-p150^Gl-1 is an enhancer of visible | adult stage phenotype of Hsap\SPTBN2^{AM.UASp.Tag:MYC}, Scer\GAL4^GMR.PF

(Lorenzo et al., 2010)

Gl[+]/DCTN1-p150^Gl-1 is an enhancer of visible phenotype of β-Spec^GM.UAS, Scer\GAL4^GMR.PF

(Lorenzo et al., 2010)

Gl[+]/DCTN1-p150^Gl-1 is an enhancer of visible | dominant phenotype of Egfr^E1

(Iyadurai et al., 2008)

DCTN1-p150^Gl-1/DCTN1-p150[+] is an enhancer of male semi-sterile phenotype of ctp^exc39

(Ghosh-Roy et al., 2004)

DCTN1-p150^Gl-1 is an enhancer of partially lethal - majority die phenotype of Lis-1^3.3.1/Lis-1^k11702

(Lei and Warrior, 2000)

DCTN1-p150^Gl-1 is an enhancer of partially lethal - majority die phenotype of Lis-1^k11702/Lis-1^7.13.1

(Lei and Warrior, 2000)

DCTN1-p150^Gl-1 is an enhancer of partially lethal - majority die phenotype of Lis-1^8.25.3/Lis-1^k11702

(Lei and Warrior, 2000)

DCTN1-p150^Gl-1 is an enhancer of partially lethal - majority die phenotype of Lis-1^3.1.2/Lis-1^k11702

(Lei and Warrior, 2000)

DCTN1-p150^Gl-1 is an enhancer of partially lethal - majority die phenotype of Lis-1^k11702/Lis-1^11.4.13

(Lei and Warrior, 2000)

DCTN1-p150^Gl-1 is an enhancer of partially lethal - majority die phenotype of Lis-1^1.2.2/Lis-1^k11702

(Lei and Warrior, 2000)

Suppressor of

Statement

Reference

Gl[+]/DCTN1-p150^Gl-1 is a suppressor of visible | dominant phenotype of Delta¹³

(Iyadurai et al., 2008)

Gl[+]/DCTN1-p150^Gl-1 is a suppressor of visible | dominant phenotype of Egfr^E1

(Iyadurai et al., 2008)

Gl[+]/DCTN1-p150^Gl-1 is a suppressor of visible phenotype of rho^Stg

(Iyadurai et al., 2008)

Other

Statement

Reference

DCTN1-p150^Gl-1, Scer\GAL4^GH146, spri^RNAi.UAS has abnormal neuroanatomy | somatic clone phenotype

(Sakuma et al., 2014)

DCTN1-p150^Gl-1, EG28^EG28/EG28[+] has abnormal neuroanatomy | dominant | adult stage phenotype

(Ma et al., 2009)

DCTN1-p150^Gl-1, ctp^DIIA82 has lethal phenotype

(Ghosh-Roy et al., 2004)

DCTN1-p150^Gl-1, ctp^ins1 has male sterile phenotype

(Ghosh-Roy et al., 2004)

Gl[+]/DCTN1-p150^Gl-1, ctp^DIIA82 has lethal phenotype

(Ghosh-Roy et al., 2004)

Gl[+]/DCTN1-p150^Gl-1, ctp^ins1 has male sterile phenotype

(Ghosh-Roy et al., 2004)

DCTN1-p150^Gl-1, sw¹ has lethal phenotype

(Boylan and Hays, 2002)

DCTN1-p150^Gl-1, Khc¹⁶/Khc[+] has paralytic | dominant | larval stage phenotype

(Martin et al., 1999)

Gl[+]/DCTN1-p150^Gl-1, Khc¹⁶ has paralytic | dominant | larval stage phenotype

(Martin et al., 1999)

Df(2L)TW119/BicD^r, DCTN1-p150^Gl-1 has lethal phenotype

(Swan et al., 1999)

DCTN1-p150^Gl-1, Lis-1^E415 has lethal phenotype

(Swan et al., 1999)

Phenotype Manifest In

Enhanced by

Statement

Reference

DCTN1-p150^Gl-1 has eye phenotype, enhanceable by dop[+]/dop¹

(Hain et al., 2014)

DCTN1-p150^Gl-1 has eye phenotype, enhanceable by Hsap\SPTBN2^{AM.UASp.Tag:MYC}/Scer\GAL4^GMR.PF

(Lorenzo et al., 2010)

DCTN1-p150^Gl-1 has ommatidium phenotype, enhanceable by Hsap\SPTBN2^{AM.UASp.Tag:MYC}/Scer\GAL4^GMR.PF

(Lorenzo et al., 2010)

DCTN1-p150^Gl-1 has eye phenotype, enhanceable by β-Spec^GM.UAS/Scer\GAL4^GMR.PF

(Lorenzo et al., 2010)

DCTN1-p150^Gl-1 has ommatidium phenotype, enhanceable by β-Spec^GM.UAS/Scer\GAL4^GMR.PF

(Lorenzo et al., 2010)

DCTN1-p150^Gl-1 has eye phenotype, enhanceable by Su(H)[+]/Su(H)^EG37

(Ma et al., 2009)

DCTN1-p150^Gl-1 has ommatidium phenotype, enhanceable by Su(H)[+]/Su(H)^EG37

(Ma et al., 2009)

DCTN1-p150^Gl-1 has rhabdomere phenotype, enhanceable by Su(H)[+]/Su(H)^EG37

(Ma et al., 2009)

DCTN1-p150^Gl-1 has eye phenotype, enhanceable by EG162[+]/EG162^EG162

(Ma et al., 2009)

DCTN1-p150^Gl-1 has giant fiber neuron phenotype, enhanceable by EG7[+]/EG7^EG7

(Ma et al., 2009)

DCTN1-p150^Gl-1 has giant fiber neuron phenotype, enhanceable by EG56^EG56/EG56[+]

(Ma et al., 2009)

DCTN1-p150^Gl-1 has giant fiber neuron phenotype, enhanceable by EG79[+]/EG79^EG79

(Ma et al., 2009)

DCTN1-p150^Gl-1 has eye phenotype, enhanceable by S[+]/S^rK134

(Iyadurai et al., 2008)

DCTN1-p150^Gl-1 has eye phenotype, enhanceable by S[+]/S¹

(Iyadurai et al., 2008)

DCTN1-p150^Gl-1 has eye phenotype, enhanceable by S⁰⁷⁰⁵⁶

(Iyadurai et al., 2008)

DCTN1-p150^Gl-1 has eye phenotype, enhanceable by S^IIN

(Iyadurai et al., 2008)

DCTN1-p150^Gl-1 has eye phenotype, enhanceable by S⁰⁵⁶⁷¹

(Iyadurai et al., 2008)

DCTN1-p150^Gl-1 has eye phenotype, enhanceable by Df(2L)S3/+

(Iyadurai et al., 2008)

DCTN1-p150^Gl-1, S[+]/S¹ has eye phenotype, enhanceable by Dhc64C[+]/Dhc64C^1-1

(Iyadurai et al., 2008)

DCTN1-p150^Gl-1 has eye photoreceptor cell & nucleus phenotype, enhanceable by sw^Dic-2/sw[+]

(Whited et al., 2004)

DCTN1-p150^Gl-1 has ommatidium phenotype, enhanceable by sw^Dic-2/sw[+]

(Boylan and Hays, 2002)

DCTN1-p150^Gl-1 has ommatidium phenotype, enhanceable by sw¹/sw[+]

(Boylan and Hays, 2002)

DCTN1-p150^Gl-1 has ommatidium phenotype, enhanceable by sw^Dic-3/sw[+]

(Boylan and Hays, 2002)

DCTN1-p150^Gl-1 has ommatidium phenotype, enhanceable by sw[+]/sw^Dic-1

(Boylan and Hays, 2002)

DCTN1-p150^Gl-1 has eye phenotype, enhanceable by Df(1)mal3/+

(Boylan et al., 2000)

DCTN1-p150^Gl-1 has ommatidium phenotype, enhanceable by Df(1)mal3/+

(Boylan et al., 2000)

DCTN1-p150^Gl-1 has eye phenotype, enhanceable by Lis-1^3.3.1/Lis-1^k11702

(Lei and Warrior, 2000)

DCTN1-p150^Gl-1 has eye phenotype, enhanceable by Lis-1^k11702/Lis-1^7.13.1

(Lei and Warrior, 2000)

DCTN1-p150^Gl-1 has eye phenotype, enhanceable by Lis-1^8.25.3/Lis-1^k11702

(Lei and Warrior, 2000)

DCTN1-p150^Gl-1 has eye phenotype, enhanceable by Lis-1^3.1.2/Lis-1^k11702

(Lei and Warrior, 2000)

DCTN1-p150^Gl-1 has eye phenotype, enhanceable by Lis-1^k11702/Lis-1^11.4.13

(Lei and Warrior, 2000)

DCTN1-p150^Gl-1 has eye phenotype, enhanceable by Dhc64C[+]/Dhc64C^6-8

(McGrail et al., 1995)

DCTN1-p150^Gl-1 has ommatidium phenotype, enhanceable by Dhc64C[+]/Dhc64C^6-8

(McGrail et al., 1995)

DCTN1-p150^Gl-1 has eye phenotype, enhanceable by Dhc64C[+]/Dhc64C^6-10

(McGrail et al., 1995)

DCTN1-p150^Gl-1 has ommatidium phenotype, enhanceable by Dhc64C[+]/Dhc64C^6-10

(McGrail et al., 1995)

NOT Enhanced by

Statement

Reference

DCTN1-p150^Gl-1 has giant fiber neuron phenotype, non-enhanceable by Su(H)[+]/Su(H)¹

(Ma et al., 2009)

DCTN1-p150^Gl-1 has ommatidium phenotype, non-enhanceable by Df(3L)10^H

(McGrail et al., 1995)

DCTN1-p150^Gl-1 has eye phenotype, non-enhanceable by Df(3L)10^H

(McGrail et al., 1995)

Suppressed by

Statement

Reference

DCTN1-p150^Gl-1 has eye phenotype, suppressible by SG13^SG13/SG13[+]

(Ma et al., 2009)

DCTN1-p150^Gl-1 has ommatidium phenotype, suppressible by SG13^SG13/SG13[+]

(Ma et al., 2009)

DCTN1-p150^Gl-1 has rhabdomere phenotype, suppressible by SG13^SG13/SG13[+]

(Ma et al., 2009)

DCTN1-p150^Gl-1 has eye phenotype, suppressible by SG46[+]/SG46^SG46

(Ma et al., 2009)

DCTN1-p150^Gl-1 has eye phenotype, suppressible by Dhc64C^8-1

(Iyadurai et al., 2008)

DCTN1-p150^Gl-1 has eye phenotype, suppressible by Dhc64C^8-1/Dhc64C⁷⁷

(Iyadurai et al., 2008)

DCTN1-p150^Gl-1 has eye photoreceptor cell & nucleus phenotype, suppressible by Khc[+]/Khc⁸

(Whited et al., 2004)

DCTN1-p150^Gl-1 has eye photoreceptor cell & nucleus phenotype, suppressible by Khc^k13219/Khc[+]

(Whited et al., 2004)

DCTN1-p150^Gl-1 has eye photoreceptor cell & nucleus phenotype, suppressible by Khc[+]/Khc^k13314

(Whited et al., 2004)

DCTN1-p150^Gl-1 has eye phenotype, suppressible by Khc[+]/Khc⁸

(Whited et al., 2004)

DCTN1-p150^Gl-1 has eye phenotype, suppressible by Khc^k13219/Khc[+]

(Whited et al., 2004)

DCTN1-p150^Gl-1 has eye phenotype, suppressible by Khc[+]/Khc^k13314

(Whited et al., 2004)

DCTN1-p150^Gl-1 has ommatidium phenotype, suppressible by Khc[+]/Khc⁸

(Whited et al., 2004)

DCTN1-p150^Gl-1 has ommatidium phenotype, suppressible by Khc^k13219/Khc[+]

(Whited et al., 2004)

DCTN1-p150^Gl-1 has ommatidium phenotype, suppressible by Khc[+]/Khc^k13314

(Whited et al., 2004)

DCTN1-p150^Gl-1 has eye phenotype, suppressible by sw^+t11

(Boylan et al., 2000)

DCTN1-p150^Gl-1 has eye phenotype, suppressible by Dp(1;Y)y⁺mal¹⁰⁶/+

(Boylan et al., 2000)

DCTN1-p150^Gl-1 has ommatidium phenotype, suppressible by sw^+t11

(Boylan et al., 2000)

DCTN1-p150^Gl-1 has ommatidium phenotype, suppressible by Dp(1;Y)y⁺mal¹⁰⁶/+

(Boylan et al., 2000)

DCTN1-p150^Gl-1 has ommatidium phenotype, suppressible by Dhc64C^6-6/Dhc64C[+]

(McGrail et al., 1995)

DCTN1-p150^Gl-1 has eye phenotype, suppressible by Dhc64C^6-6/Dhc64C[+]

(McGrail et al., 1995)

DCTN1-p150^Gl-1 has eye phenotype, suppressible by Dhc64C[+]/Dhc64C¹⁰²

(Harte and Kankel, 1982)

DCTN1-p150^Gl-1 has adult optic lobe phenotype, suppressible by Dhc64C[+]/Dhc64C¹⁰²

(Harte and Kankel, 1982)

DCTN1-p150^Gl-1 has eye phenotype, suppressible by Su(Gl)77[+]/Su(Gl)160¹⁶⁰

(Harte and Kankel, 1982)

DCTN1-p150^Gl-1 has adult optic lobe phenotype, suppressible by Su(Gl)77[+]/Su(Gl)160¹⁶⁰

(Harte and Kankel, 1982)

DCTN1-p150^Gl-1 has eye phenotype, suppressible by Su(Gl)27[+]/Su(Gl)27¹

(Harte and Kankel, 1982)

DCTN1-p150^Gl-1 has adult optic lobe phenotype, suppressible by Su(Gl)27[+]/Su(Gl)27¹

(Harte and Kankel, 1982)

DCTN1-p150^Gl-1 has eye phenotype, suppressible by Su(Gl)57[+]/Su(Gl)57¹

(Harte and Kankel, 1982)

DCTN1-p150^Gl-1 has adult optic lobe phenotype, suppressible by Su(Gl)57[+]/Su(Gl)57¹

(Harte and Kankel, 1982)

NOT suppressed by

Statement

Reference

DCTN1-p150^Gl-1, S[+]/S¹ has eye phenotype, non-suppressible by Dhc64C⁷⁷/Su(Gl)77[+]

(Iyadurai et al., 2008)

DCTN1-p150^Gl-1, S[+]/S¹ has eye phenotype, non-suppressible by Dhc64C[+]/Dhc64C^8-1

(Iyadurai et al., 2008)

DCTN1-p150^Gl-1, S[+]/S¹ has eye phenotype, non-suppressible by Dhc64C^8-1/Dhc64C⁷⁷

(Iyadurai et al., 2008)

DCTN1-p150^Gl-1 has ommatidium phenotype, non-suppressible by Df(3L)10^H

(McGrail et al., 1995)

DCTN1-p150^Gl-1 has eye phenotype, non-suppressible by Df(3L)10^H

(McGrail et al., 1995)

Enhancer of

Statement

Reference

DCTN1-p150^Gl-1 is an enhancer of membrane | embryonic stage 5 phenotype of dop¹

(Hain et al., 2014)

DCTN1-p150^Gl-1 is an enhancer | somatic clone of adult antennal lobe projection neuron DL1 adPN | somatic clone phenotype of Strip^dogi

(Sakuma et al., 2014)

DCTN1-p150^Gl-1 is an enhancer of eye phenotype of Hsap\SPTBN2^{AM.UASp.Tag:MYC}, Scer\GAL4^GMR.PF

(Lorenzo et al., 2010)

DCTN1-p150^Gl-1 is an enhancer of ommatidium phenotype of Hsap\SPTBN2^{AM.UASp.Tag:MYC}, Scer\GAL4^GMR.PF

(Lorenzo et al., 2010)

Gl[+]/DCTN1-p150^Gl-1 is an enhancer of eye phenotype of β-Spec^GM.UAS, Scer\GAL4^GMR.PF

(Lorenzo et al., 2010)

Gl[+]/DCTN1-p150^Gl-1 is an enhancer of ommatidium phenotype of β-Spec^GM.UAS, Scer\GAL4^GMR.PF

(Lorenzo et al., 2010)

Gl[+]/DCTN1-p150^Gl-1 is an enhancer of eye phenotype of Egfr^E1

(Iyadurai et al., 2008)

Gl[+]/DCTN1-p150^Gl-1 is an enhancer of cystic bulge phenotype of ctp^exc39

(Ghosh-Roy et al., 2005)

Gl[+]/DCTN1-p150^Gl-1 is an enhancer of nucleus & spermatid phenotype of ctp^exc39

(Ghosh-Roy et al., 2005)

Gl[+]/DCTN1-p150^Gl-1 is an enhancer of cystic bulge phenotype of ctp^ins1

(Ghosh-Roy et al., 2005)

Gl[+]/DCTN1-p150^Gl-1 is an enhancer of nucleus & spermatid phenotype of ctp^ins1

(Ghosh-Roy et al., 2005)

Gl[+]/DCTN1-p150^Gl-1 is an enhancer of spermatid cyst phenotype of ctp^ins1

(Ghosh-Roy et al., 2004)

Gl[+]/DCTN1-p150^Gl-1 is an enhancer of spermatocyte fusome phenotype of ctp^ins1

(Ghosh-Roy et al., 2004)

Gl[+]/DCTN1-p150^Gl-1 is an enhancer of posterior fascicle & axon phenotype of Khc¹⁶

(Martin et al., 1999)

NOT Enhancer of

Statement

Reference

Gl[+]/DCTN1-p150^Gl-1 is a non-enhancer of organism | cleavage stage | maternal effect phenotype of αTub67C^kav-21g

(Gaspar and Szabad, 2009)

Suppressor of

Statement

Reference

Gl[+]/DCTN1-p150^Gl-1 is a suppressor of wing vein L2 phenotype of Delta¹³

(Iyadurai et al., 2008)

Gl[+]/DCTN1-p150^Gl-1 is a suppressor of wing vein L2 phenotype of Egfr^E1

(Iyadurai et al., 2008)

Gl[+]/DCTN1-p150^Gl-1 is a suppressor of wing | ectopic phenotype of rho^Stg

(Iyadurai et al., 2008)

Gl[+]/DCTN1-p150^Gl-1 is a suppressor of aster | embryonic cycle 5 phenotype of CycB^+t10

(Ji et al., 2002)

Gl[+]/DCTN1-p150^Gl-1 is a suppressor of aster | embryonic cycle 6 phenotype of CycB^+t10

(Ji et al., 2002)

Gl[+]/DCTN1-p150^Gl-1 is a suppressor of aster | embryonic cycle 7 phenotype of CycB^+t10

(Ji et al., 2002)

NOT Suppressor of

Statement

Reference

Gl[+]/DCTN1-p150^Gl-1 is a non-suppressor of organism | maternal effect | cleavage stage phenotype of αTub67C^kav-21g

(Gaspar and Szabad, 2009)

Other

Statement

Reference

DCTN1-p150^Gl-1, Scer\GAL4^GH146, spri^RNAi.UAS has adult antennal lobe projection neuron DL1 adPN | somatic clone phenotype

(Sakuma et al., 2014)

DCTN1-p150^Gl-1, EG28^EG28/EG28[+] has giant fiber neuron phenotype

(Ma et al., 2009)

DCTN1-p150^Gl-1, ctp^exc39 has spermatocyte fusome phenotype

(Ghosh-Roy et al., 2004)

Gl[+]/DCTN1-p150^Gl-1, ctp^exc39 has spermatocyte fusome phenotype

(Ghosh-Roy et al., 2004)

DCTN1-p150^Gl-1, Lis-1^3.3.1/Lis-1^k11702 has macrochaeta phenotype

(Lei and Warrior, 2000)

DCTN1-p150^Gl-1, Lis-1^3.3.1/Lis-1^k11702 has abdominal tergite phenotype

(Lei and Warrior, 2000)

DCTN1-p150^Gl-1, Lis-1^3.3.1/Lis-1^k11702 has microchaeta & abdomen | ventral phenotype

(Lei and Warrior, 2000)

DCTN1-p150^Gl-1, Lis-1^k11702/Lis-1^7.13.1 has macrochaeta phenotype

(Lei and Warrior, 2000)

DCTN1-p150^Gl-1, Lis-1^k11702/Lis-1^7.13.1 has abdominal tergite phenotype

(Lei and Warrior, 2000)

DCTN1-p150^Gl-1, Lis-1^k11702/Lis-1^7.13.1 has microchaeta & abdomen | ventral phenotype

(Lei and Warrior, 2000)

DCTN1-p150^Gl-1, Lis-1^8.25.3/Lis-1^k11702 has macrochaeta phenotype

(Lei and Warrior, 2000)

DCTN1-p150^Gl-1, Lis-1^8.25.3/Lis-1^k11702 has abdominal tergite phenotype

(Lei and Warrior, 2000)

DCTN1-p150^Gl-1, Lis-1^8.25.3/Lis-1^k11702 has microchaeta & abdomen | ventral phenotype

(Lei and Warrior, 2000)

DCTN1-p150^Gl-1, Lis-1^3.1.2/Lis-1^k11702 has macrochaeta phenotype

(Lei and Warrior, 2000)

DCTN1-p150^Gl-1, Lis-1^3.1.2/Lis-1^k11702 has abdominal tergite phenotype

(Lei and Warrior, 2000)

DCTN1-p150^Gl-1, Lis-1^3.1.2/Lis-1^k11702 has microchaeta & abdomen | ventral phenotype

(Lei and Warrior, 2000)

DCTN1-p150^Gl-1, Lis-1^k11702/Lis-1^11.4.13 has macrochaeta phenotype

(Lei and Warrior, 2000)

DCTN1-p150^Gl-1, Lis-1^k11702/Lis-1^11.4.13 has abdominal tergite phenotype

(Lei and Warrior, 2000)

DCTN1-p150^Gl-1, Lis-1^k11702/Lis-1^11.4.13 has microchaeta & abdomen | ventral phenotype

(Lei and Warrior, 2000)

DCTN1-p150^Gl-1, Lis-1^1.2.2/Lis-1^k11702 has macrochaeta phenotype

(Lei and Warrior, 2000)

DCTN1-p150^Gl-1, Lis-1^1.2.2/Lis-1^k11702 has abdominal tergite phenotype

(Lei and Warrior, 2000)

DCTN1-p150^Gl-1, Lis-1^1.2.2/Lis-1^k11702 has microchaeta & abdomen | ventral phenotype

(Lei and Warrior, 2000)

DCTN1-p150^Gl-1, Df(3L)10^H/+ has posterior fascicle & axon phenotype

(Martin et al., 1999)

DCTN1-p150^Gl-1, Dhc64C[+]/Dhc64C^ek1 has posterior fascicle & axon phenotype

(Martin et al., 1999)

Gl[+]/DCTN1-p150^Gl-1, Dhc64C^ek1 has posterior fascicle & axon phenotype

(Martin et al., 1999)

Additional Comments

Genetic Interactions

Statement

Reference

The defect in membrane growth in dop¹ embryos is strongly enhanced by Gl¹.

(Hain et al., 2014)

The axon elongation and dendrite branching defects seen in Strip^dogi DL1 olfactory projection neuron single-cell clones are more severe if the cells are also homozygous for Gl¹. The axon fails to exit the antennal lobe in 15.6% of cases.

Gl¹ DL1 olfactory projection neuron single-cell clones expressing spri^{dsRNA.shRNA.Scer\UAS} under the control of Scer\GAL4^GH146 show axon elongation and dendrite branching defects. The axon fails to exit the antennal lobe in 38.9% of cases.

(Sakuma et al., 2014)

Su(H)^EG37 dominantly enhances the eye phenotype caused by Gl¹, resulting in an increase in bristles and an increase in ommatidial fusion and disorganisation. There is increased disruption of accessory cells and rhabdomeres are often fused.

SG13^SG13 dominantly suppresses the eye phenotype caused by Gl¹, with ommatidia showing a more ordered, regular pattern and with each ommatidium often having the correct array of rhabdomeres.

The fraction of giant fiber axons that lack the characteristic terminal bend in Gl¹/+ flies is increased if they are also heterozygous for EG7^EG7, EG56^EG56 or EG79^EG79.

Only 3% of giant fiber axons in Gl¹/+ ; EG28^EG28/+ double heterozygotes lack the characteristic terminal bend, but the axons often show ectopic branching.

The electrophysiological defects seen in the giant fiber system of Gl¹/+ adults are enhanced if they are also heterozygous for one of EG149^EG149, EG162^EG162, Su(H)^EG37, EG28^EG28, EG165^EG165, EG7^EG7, EG56^EG56 or EG79^EG79; the response latencies are significantly increased and the double heterozygous flies show poor following.

Su(H)¹/+ does not enhance the morphological or electrophysiological defects of the giant fiber axons of Gl¹/+ flies.

(Ma et al., 2009)

S^rK134/+ enhances the rough eye phenotype of Gl¹/+ flies, producing a significant reduction in eye size and disruption of the hexagonal packing of the ommatidia.

Df(2L)S3/+ enhances the rough eye phenotype of Gl¹/+ flies, resulting in very small, narrow, rough eyes with a reduced number of ommatidia.

The S¹ mutation overcomes the suppression of the Gl¹ rough eye phenotype by Dhc64C⁷⁷ or Dhc64C^8-1, so that triple heterozygotes have an enhanced rough eye phenotype compared to Gl¹ single heterozygotes.

Gl¹ Dhc64C⁷⁷ Dhc64C^8-1 flies have completely wild-type eyes.

The enhanced rough eye phenotype of Gl¹/+ S¹/+ flies is not suppressed by Dhc64C⁷⁷/Dhc64C^8-1.

The abnormal broadening of wing vein L2 at the wing margin which is seen in Dl¹³/+ and Egfr^E1/+ flies is suppressed by Gl¹/+.

The extra wing vein phenotype caused by rho^Stg is partially suppressed by Gl¹/+.

(Iyadurai et al., 2008)

The ctp^exc39/Y and ctp^ins1/Y nuclear bundles and individualization complex phenotype is dominantly enhanced by Gl¹.

(Ghosh-Roy et al., 2005)

The sterility of ctp^exc39 males is further reduced when flies carry one copy of Gl¹. The sterility of ctp^ins1 males is enhanced to 100% when they are heterozygous for Gl¹. The ctp^DIIA82 mutation is lethal in combination with one copy of Gl¹. The total number of elongation cones (ECs) per testis is reduced in ctp^exc39 mutants that carry one copy of Gl¹; some of these ECs are deformed and the average cyst length is shorter than in ctp^exc39 single mutants.

(Ghosh-Roy et al., 2004)

The area of the retina of late third instar Gl¹/+ larvae devoid of nuclei is significantly increased by sw^Dic-2/+. This is not due to cell death, but instead due increased migration of nuclei into the optic stalk. The Gl¹/+ adult eye phenotype and the loss of photoreceptor nuclei from the retina in late third instar Gl¹/+ larvae are partially suppressed by Khc^k13219/+ or Khc^k13314/+ and almost completely suppressed by Khc⁸/+.

(Whited et al., 2004)

The rough eye phenotypes of Gl¹/+ flies is dominantly enhanced by sw^Dic-1, sw^Dic-2 or sw^Dic-3.

(Boylan and Hays, 2002)

The Gl¹/+ rough eye phenotype is suppressed by sw^+t11 or Dp(1;Y)y⁺mal¹⁰⁶ and enhanced by Df(1)mal3.

(Boylan et al., 2000)

The slight loss of viability phenotype seen in Lis-1^k11702/Lis-1^3.3.1, Lis-1^k11702/Lis-1^3.1.2, Lis-1^k11702/Lis-1^8.25.3, Lis-1^k11702/Lis-1^11.4.13 or Lis-1^k11702/Lis-1^7.13.1, is enhanced by the addition of Gl¹. The adult escapers from these crosses generally do not survive more than a few days. The addition of these Lis-1 transheterozygote combinations enhances the eye phenotype seen in Gl¹ flies. In addition scutellar bristles of escapers flies are reduced in size and frequently lost. Most adult escapers lack bristles on the ventral side of the abdomen, and in many animals abdominal tergites are completely absent in one or more segments. In addition the scutellar bristles of escaper flies are reduced in size and often lost.

(Lei and Warrior, 2000)

Gl¹ shows a posterior paralysis phenotype in larvae in double heterozygous combination with Khc¹⁶. Dhc64C^ek1 Gl¹ double heterozygous larvae do not show a posterior paralysis phenotype. Some axonal swellings are seen in the segmental nerves of heterozygous Khc¹⁶ larvae. The number of axonal swellings is dramatically increased if the larvae are also heterozygous for Gl¹. The axon swellings seen in double heterozygotes are rescued by Khc^+t7.5. A slight increase in the number of axonal swellings in the segmental nerves is seen in Gl¹/Df(3L)10^H or Dhc64C^ek1/+ ; Gl¹/+ double heterozygous larvae compared to single heterozygotes.

(Martin et al., 1999)

Expression of Hsap\CDKN1A^GMR.PH, which blocks the second mitotic wave, substantially reduces the number of mispositioned nuclei in Gl¹ mutants suggesting that cell division at the second mitotic wave is not a prerequisite for nuclear mispositioning. Substantial cell death is also seen when Hsap\CDKN1A^GMR.PH is expressed in Gl¹ mutants suggesting the block in second mitotic wave, nuclear mispositioning and cell death are independent events.

(Fan and Ready, 1997)

The Gl¹/+ rough eye phenotype is dominantly suppressed by Dhc64C^6-6; ommatidia are shaped normally except in the most posterior region of the eye. The rough eye phenotype is not altered by Df(3L)10^H. The rough eye phenotype is dominantly enhanced by Dhc64C^6-8 and Dhc64C^6-10, in both cases the eyes are reduced in size and ommatidia are frequently fused. The enhancement of the Gl¹ phenotype by Dhc64C^6-8 and Dhc64C^6-10 is reversed if the flies also carry a copy of Dhc64C^+tDN17.

(McGrail et al., 1995)

Dhc64C¹⁰² is a dominant suppressor of the Gl¹ phenotype in the eye. More normal facet arrays are seen in the anterior than in the posterior part of the eye in the double heterozygous flies. The optic lobe phenotype of Gl¹ is also suppressed in the double heterozygote, with the strongest defect being that the lamina cell body layer is thicker than normal in the posterior region and the lamina neuropile is somewhat misshapen, particularly anteriorly. The medulla is abnormally rotated, with its posterior edge directly apposed to the lamina, but it is more normally organised than in the Gl¹ single mutant.

Su(Gl)160¹⁶⁰ is a dominant suppressor of the Gl¹ phenotype in the eye and the optic lobe. More normal facet arrays are seen in the anterior than in the posterior part of the eye in the double heterozygous flies.

Su(Gl)27¹ is a dominant suppressor of Gl¹, which results in an almost wild-type phenotype in the eye and optic lobe of double heterozygotes at 29[o]C (the optic lobe is very nearly normal at this temperature but the lamina cell body is thicker than normal and the lamina neuropil is slightly irregular in contour). At 18[o]C, the eyes of double heterozygotes are smaller than normal and there are some small facets scattered throughout the eye. In addition, the facets are not packed as tightly together as normal, and smooth pigmented material can be seen separating facets from each other.

(Harte and Kankel, 1982)

Xenogenetic Interactions

Statement

Reference

44% of third instar larvae expressing one copy of Hsap\SPTBN2^{AM.Scer\UAS.P\T.T:Hsap\MYC} under the control of Scer\GAL4^elav.PU in a heterozygous Gl¹ mutant background exhibit a "tail flip" phenotype due to posterior paralysis. 18% of larvae exhibit paralysis in the absence of the Scer\GAL4^elav.PU driver.

Expression of one copy of Hsap\SPTBN2^{AM.Scer\UAS.P\T.T:Hsap\MYC} under the control of Scer\GAL4^GMR.PF in a Gl¹/+ mutant background enhances the rough eye and ommatidial disorganisation phenotypes seen in either mutant alone. Eyes from double mutant flies are reduced in size and show a dramatic roughness of the eye surface.

Expression of one copy of β-Spec^GM.Scer\UAS under the control of Scer\GAL4^GMR.PF in a Gl¹/+ mutant background enhances the rough eye and ommatidial disorganisation phenotypes seen in either mutant alone. Eyes from double mutant flies are reduced in size and show a dramatic roughness of the eye surface.

(Lorenzo et al., 2010)

Complementation and Rescue Data

Comments

Images (1)

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

Mutant

Wild-type

Stocks (11)

Bloomington

510

DCTN1-p150^Gl-1 Sb¹/LVM

35524

w¹¹¹⁸; DCTN1-p150^Gl-1/TM3, P{sChFP}3, Sb¹

98340

y¹ w^*; wg^Sp-1/CyO; DCTN1-p150^Gl-1/TM6

98341

w^*; wg^Sp-1/CyO; DCTN1-p150^Gl-1/TM6B, Tb¹

504

amd²¹ Bl¹/CyO; DCTN1-p150^Gl-1/TM3, Sb¹ Ser¹

5750

w^*; DCTN1-p150^Gl-1 Diap1^th-1 st¹ P{FRT(w^hs)}2A/TM3, Sb¹ Ser¹

Kyoto

105950

DCTN1-p150^Gl-1 Sb¹/LVM

107307

In(3L)D, D¹/DCTN1-p150^Gl-1

107634

DCTN1-p150^Gl-1 Sb¹ H¹/In(3L)P, In(3R)P

105944

amd²¹ Bl¹ / CyO; DCTN1-p150^Gl-1 / TM3, Sb¹ Ser¹

108406

w^*; DCTN1-p150^Gl-1 Diap1^th-1 st¹ P{FRT(w^hs)}2A/TM3, Sb¹ Ser¹

Notes on Origin

Discoverer

Ives, 31 June 1931.

External Crossreferences and Linkouts ( 0 )

Synonyms and Secondary IDs (8)

Reported As

Symbol Synonym

DCTN1-p150¹

DCTN1-p150^Gl-1

(Swaroop et al., 1986, Swaroop et al., 1985)

Gl¹

(Ermanoska et al., 2014, Hain et al., 2014, Sakuma et al., 2014, Lloyd et al., 2012, Rawson et al., 2012, Lorenzo et al., 2010, Anderson et al., 2009, Christensen et al., 2009.2.28, Gaspar and Szabad, 2009, Ma et al., 2009, Iyadurai et al., 2008, Li et al., 2008, Pilling et al., 2006, Delanoue and Davis, 2005)

Gl^31f5

(Plough and Ives, 1934)

Glu¹

(Wehr et al., 2006, Mosley-Bishop et al., 1999)

Glued¹

(Chang et al., 2013, Ghosh-Roy et al., 2005, Roy and Ray, 2001)

l(3)Gl¹

(Harte and Kankel, 1982)

Name Synonyms

Glued1

(Schottenfeld-Roames and Ghabrial, 2012, Li et al., 2008)

Secondary FlyBase IDs

References (65)

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