FlyBase Allele Report: Dmel\Dysb[e01028]

Dysb^e01028 homozygous wandering third instar larvae display a significantly increased rate of depletion and a significantly decreased rate of recovery of the synaptic vesicle pool upon high-frequency stimulation of the neuromuscular junction, as compared to controls.

Under rest conditions, the neuromuscular junction presynaptic boutons of Dysb^e01028 homozygous wandering third instar larvae show no significant differences in the size and density of endosomes, in the intensity of presynaptic T-bars, in the size, number and density of synaptic vesicles, and in the density of tubular endosomes, but show a significant increase in the density of cisternal endosomes, as compared to controls. Stimulation with 90mM potassium chloride leads to a significant decrease in the size and density of Dysb^e01028 presynaptic bouton endosomes as compared to both unstimulated mutants and stimulated wild-type controls, and a significant decrease in the density of Dysb^e01028 presynaptic bouton vesicles as compared to unstimulated mutants but not to stimulated wild-type controls, whereas this stimulation has no significant effect either in the size and density of endosomes or in the density of synaptic vesicles in wild-type presynaptic boutons; stimulation with potassium chloride also leads to the density of cisternal endosomes and tubular endosomes in Dysb^e01028 presynaptic boutons to be significantly decreased and increased, respectively, as compared to both unstimulated mutants and stimulated wild-type controls, whereas this stimulation leads to a significant increase in the density of cisternal endosomes, but not tubular endosomes, in wild-type presynaptic bouton endosomes.

(Chen et al., 2017)

Dysb^e01028 heterozygote third instar larvae do not show any defects in the number or size of boutons nor the axonal branching at neuromusclular junctions.

(Furukubo-Tokunaga et al., 2016)

Dysb^e01028 homozygous as well as heterozygous mutant third instar larvae display increased number of boutons on neuromuscular junctions compared to controls, but not when the larvae are kept on 'DD' food (after Dickman and Davis, 2009) as it induces higher number of boutons in the control flies and this is not elevated further in Dysb^e01028 mutants. Heterozygous larvae also show reduced number of dendritic branches as well as the total dendrite length in class IV dendritic arborizing neurons.

(Gokhale et al., 2016)

Wild-type synapses increase their quantal content following Phillanthatoxin-433 (PhTx-433) treatment. In contrast, Dysb^e01028 animals do not display a homeostatic increase in quantal content.

(Gokhale et al., 2015)

Dysb^e01028 has no effect on excitatory junction potential (EJP) amplitude or miniature EJP frequency compared to controls. mEJP amplitude is not altered in these flies. Homozygous Dysb^e01028 mutant flies fail to show the increase in quantal content normally observed in response to philanotoxin, and this phenotype is not seen in heterozygotes. The rate of vesicle depletion at both low and high frequency stimulation is similar to controls.

Expression of Dysb^Scer\UAS.cDa under the control of Scer\GAL4^elav-C155 in a Dysb^e01028/+ mutant background has no effect on excitatory junction potential (EJP) amplitude or miniature EJP frequency compared to controls.

Homozygous Dysb^e01028 mutant flies exhibit deficits in short term olfactory habituation. This phenotype is not observed in the heterozygote.

Dysb^e01028/Df(3L)BSC416 mutant flies exhibit deficits in short term olfactory habituation. This phenotype is not observed in either heterozygote.

(Mullin et al., 2015)

Dysb^e01028 heterozygotes do not exhibit defects in synaptic homeostasis.

(Dickman et al., 2012)

Homozygous dysb^e01028 mutant larvae show significantly attenuated excitatory junctional currents in the neuromuscular junction compared to controls. This attenuation is seen at various calcium concentrations and without significant morphological changes.

The dopamine concentration in dysb^e01028 mutant heads is around twofold of that in wild type cells.

Homozygous dysb^e01028 mutant adult flies exhibit defects in memory retention following exposure to an odor previously associated without electric shock. Memory is affected at both 1h and 3h after single session training and 24 hours after repetitive training. The sensorimotor responses necessary for performing the learning task are not altered. This phenotype can be rescued by feeding flies with the NMDA receptor agonist, glycine.

dysb^e01028 mutant flies show elevated activity in response to light taps on the container compared to wild type flies of the same age. This hyperactivity can be significantly rescued by feeding flies resperine or α-methyl-p-tyrosine (AMPT).

dysb^e01028 mutant flies do not exhibit the strong wild type bias towards females, courting male flies as well as female flies. No phenotypes are seen in either of the single heterozygotes. This phenotype can be significantly rescued by feeding flies resperine or α-methyl-p-tyrosine (AMPT).

(Shao et al., 2011)

Homozygous and dysb^e01028/Df(3L)BSC416 neuromuscular junctions show a complete absence of homeostatic compensation (increase in quantal content) after treatment with philanthotoxin-433 for 10 minutes.

Bouton number and active zone density at the neuromuscular junction are normal in mutant larvae.

Homozygous larvae show no significant change in baseline synaptic transmission in 0.5mM extracellular Ca[2+] compared to controls. However, at reduced extracellular Ca[2+] (0.2 to 0.4mM) , baseline synaptic transmission is significantly impaired in the mutants relative to controls. At reduced extracellular Ca[2+] both paired-pulse facilitation and facilitation that occurs during a prolonged stimulus train are increased in the mutants.

(Dickman and Davis, 2009)

External Data

Linkouts

Interactions

Show genetic interaction network for Enhancers & Suppressors

Phenotypic Class

NOT Enhanced by

Statement

Reference

Dysb^e01028 has abnormal neuroanatomy | third instar larval stage phenotype, non-enhanceable by Arpc1^Q25sd/Arpc1[+]

(Gokhale et al., 2016)

Suppressed by

Statement

Reference

Dysb^e01028 has abnormal neuroanatomy | third instar larval stage phenotype, suppressible by Arpc1^Q25sd/Arpc1[+]

(Gokhale et al., 2016)

Dysb^e01028 has abnormal neurophysiology | drug conditional phenotype, suppressible by Scer\GAL4^elav-C155/comt^UAS.Tag:FLAG

(Gokhale et al., 2015)

Dysb^e01028 has abnormal neurophysiology | larval stage phenotype, suppressible by Scer\GAL4^elav-C155/Hsap\DTNBP1^UAS.cSa

(Shao et al., 2011)

Dysb^e01028 has abnormal memory | adult stage phenotype, suppressible by Scer\GAL4^elav-C155/Hsap\DTNBP1^UAS.cSa

(Shao et al., 2011)

Dysb^e01028 has abnormal locomotor behavior | adult stage phenotype, suppressible by Scer\GAL4^repo/Hsap\DTNBP1^UAS.cSa

(Shao et al., 2011)

NOT suppressed by

Statement

Reference

Dysb^e01028 has abnormal neurophysiology | wandering third instar larval stage | conditional phenotype, non-suppressible by Scer\GAL4^RapGAP1-OK6/Pldn^UAS.cCa

(Chen et al., 2017)

Dysb^e01028 has abnormal neuroanatomy | third instar larval stage phenotype, non-suppressible by Arpc1^Q25sd/Arpc1[+]

(Gokhale et al., 2016)

Dysb^e01028 has abnormal neurophysiology phenotype, non-suppressible by Scer\GAL4^elav-C155/cac^UAS.EGFP

(Dickman and Davis, 2009)

Enhancer of

Statement

Reference

Dysb[+]/Dysb^e01028 is an enhancer of abnormal neuroanatomy | third instar larval stage phenotype of Hsap\DISC1^UAS.Tag:HA, Scer\GAL4^Tub.PU

(Furukubo-Tokunaga et al., 2016)

NOT Enhancer of

Statement

Reference

CG6856[+]/Dysb^e01028 is a non-enhancer of abnormal neurophysiology | dominant phenotype of cac^S

(Dickman and Davis, 2009)

Suppressor of

Statement

Reference

Dysb^e01028/Dysb^e01028 is a suppressor of abnormal neurophysiology | larval stage phenotype of Madm^UAS.EGFP, Scer\GAL4^{GluRIIB-MI03631-TG4.2}

(Mushtaq et al., 2022)

Dysb[+]/Dysb^e01028 is a suppressor of abnormal neuroanatomy | third instar larval stage phenotype of Arpc1^Q25sd

(Gokhale et al., 2016)

Dysb[+]/Dysb^e01028 is a suppressor of abnormal neurophysiology | dominant phenotype of Blos1^ex65

(Mullin et al., 2015)

Dysb[+]/Dysb^e01028 is a suppressor of abnormal neuroanatomy | dominant phenotype of Blos1^ex65

(Mullin et al., 2015)

Dysb[+]/Dysb^e01028 is a suppressor of abnormal neurophysiology | dominant phenotype of Blos1^EY06269

(Mullin et al., 2015)

Dysb[+]/Dysb^e01028 is a suppressor of abnormal neuroanatomy | dominant phenotype of Blos1^EY06269

(Mullin et al., 2015)

NOT Suppressor of

Statement

Reference

Scer\GAL4^elav-C155, Dysb[+], Dysb^UAS.cDa, Dysb^e01028 is a non-suppressor of abnormal neurophysiology | dominant phenotype of Blos1^EY06269

(Mullin et al., 2015)

Other

Statement

Reference

Df(3R)Exel7283/Madm^4S3, Dysb^e01028, Madm^UAS.EGFP, Scer\GAL4^{GluRIIB-MI03631-TG4.2} has abnormal neuroanatomy | larval stage phenotype

(Mushtaq et al., 2022)

Df(3R)Exel7283/Madm^4S3, Dysb^e01028, Madm^UAS.EGFP, Scer\GAL4^{GluRIIB-MI03631-TG4.2} has abnormal neurophysiology | larval stage phenotype

(Mushtaq et al., 2022)

Dysb^e01028, Madm^GD7155, Scer\GAL4^elav-C155 has abnormal neurophysiology | larval stage phenotype

(Mushtaq et al., 2022)

Blos1[+]/Blos1^ex2, Dysb^e01028 has abnormal learning phenotype

(Mullin et al., 2015)

Blos1[+]/Blos1^ex65, Dysb^e01028 has abnormal learning phenotype

(Mullin et al., 2015)

Blos1^EY06269, Dysb[+]/Dysb^e01028 has abnormal neurophysiology phenotype

(Mullin et al., 2015)

dysb[+]/Dysb^e01028, e¹ has abnormal locomotor behavior | dominant | adult stage phenotype

(Shao et al., 2011)

dysb[+]/Dysb^e01028, e¹ has abnormal courtship behavior | dominant | adult stage phenotype

(Shao et al., 2011)

Dysb^e01028, GluRIIA^SP16 has abnormal neurophysiology phenotype

(Dickman and Davis, 2009)

Phenotype Manifest In

NOT Enhanced by

Statement

Reference

Dysb^e01028 has larval multidendritic class IV neuron | third instar larval stage phenotype, non-enhanceable by Arpc1^Q25sd/Arpc1[+]

(Gokhale et al., 2016)

Dysb^e01028 has dendrite | third instar larval stage phenotype, non-enhanceable by Arpc1^Q25sd/Arpc1[+]

(Gokhale et al., 2016)

Suppressed by

Statement

Reference

Dysb^e01028 has NMJ bouton | increased number | third instar larval stage phenotype, suppressible by Arpc1^Q25sd/Arpc1[+]

(Gokhale et al., 2016)

Dysb^e01028 has embryonic/larval neuromuscular junction | larval stage phenotype, suppressible by Scer\GAL4^elav-C155/Hsap\DTNBP1^UAS.cSa

(Shao et al., 2011)

NOT suppressed by

Statement

Reference

Dysb^e01028 has synapse | wandering third instar larval stage | conditional phenotype, non-suppressible by Scer\GAL4^RapGAP1-OK6/Pldn^UAS.cCa

(Chen et al., 2017)

Dysb^e01028 has larval multidendritic class IV neuron | third instar larval stage phenotype, non-suppressible by Arpc1^Q25sd/Arpc1[+]

(Gokhale et al., 2016)

Dysb^e01028 has dendrite | third instar larval stage phenotype, non-suppressible by Arpc1^Q25sd/Arpc1[+]

(Gokhale et al., 2016)

Enhancer of

Statement

Reference

Dysb[+]/Dysb^e01028 is an enhancer of NMJ bouton | third instar larval stage phenotype of Hsap\DISC1^UAS.Tag:HA, Scer\GAL4^Tub.PU

(Furukubo-Tokunaga et al., 2016)

Dysb[+]/Dysb^e01028 is an enhancer of embryonic/larval neuromuscular junction | third instar larval stage phenotype of Hsap\DISC1^UAS.Tag:HA, Scer\GAL4^Tub.PU

(Furukubo-Tokunaga et al., 2016)

NOT Enhancer of

Statement

Reference

Dysb[+]/Dysb^e01028 is a non-enhancer of axon | third instar larval stage phenotype of Hsap\DISC1^UAS.Tag:HA, Scer\GAL4^Tub.PU

(Furukubo-Tokunaga et al., 2016)

Suppressor of

Statement

Reference

Dysb^e01028/Dysb^e01028 is a suppressor of embryonic/larval neuromuscular junction | larval stage phenotype of Madm^UAS.EGFP, Scer\GAL4^{GluRIIB-MI03631-TG4.2}

(Mushtaq et al., 2022)

Dysb[+]/Dysb^e01028 is a suppressor of NMJ bouton | increased number | third instar larval stage phenotype of Arpc1^Q25sd

(Gokhale et al., 2016)

Dysb[+]/Dysb^e01028 is a suppressor of NMJ bouton | increased number phenotype of Blos1^ex65

(Mullin et al., 2015)

Dysb[+]/Dysb^e01028 is a suppressor of NMJ bouton | increased number phenotype of Blos1^EY06269

(Mullin et al., 2015)

Other

Statement

Reference

Additional Comments

Genetic Interactions

Statement

Reference

The expression of Pldn^Scer\UAS.cCa under the control of Scer\GAL4^RapGAP1-OK6 does not suppress either the increased rate of depletion or the decreased rate of recovery of the synaptic vesicle pool upon high-frequency stimulation of the neuromuscular junction exhibited by Dysb^e01028 homozygous wandering third instar larvae; homozygosity for Dysb^e01028 also does not significantly affect the total quanta release during neurotransmission across shi¹ homozygous wandering third instar larval neuromuscular junctions at the restrictive 32[o]C temperature.

(Chen et al., 2017)

The increased number of boutons on neuromuscular junctions observed in third instar larvae mutant for any of the following alleles: Arpc1^Q25sd (in heterozygous state), Pldn^del (homozygous) or Dysb^e01028 (either homozygous or heterozygous) is restored to wild-type levels in both Arpc1^Q25sd/+;Pldn^del/+ and Arpc1^Q25sd/+;Dysb^e01028/+ double heterozygotes.

The reduced number of dendritic branches as well as the total dendrite length in class IV dendritic arborizing neurons characteristic for Dysb^e01028 heterozugous larvae is not modified by combination with a single copy of Arpc1^Q25sd.

(Gokhale et al., 2016)

Presynaptic expression of comt^{Scer\UAS.T:Zzzz\FLAG} using Scer\GAL4^elav-C155 restores the homeostatic quantal content increase to wild-type levels in Dysb^e01028 mutants.

(Gokhale et al., 2015)

Blos1^EY06269 Dysb^e01028 double heterozygotes have no effect on excitatory junction potential (EJP) amplitude or miniature EJP frequency compared to controls. Synaptic vesicles are similar in size to controls. The increase in quantal content normally observed in response to philanotoxin is not seen. One copy of Dysb^e01028 suppresses the dominant changes in mEJP amplitude and quantal content seen in Blos1^EY06269/+ mutant NMJs. The increase in bouton number seen in Blos1^EY06269/+ NMJs is also suppressed.

Expression of Dysb^Scer\UAS.cDa under the control of Scer\GAL4^elav-C155 in a Blos1^EY06269/+; Dysb^e01028/+ mutant background has no effect on excitatory junction potential (EJP) amplitude or miniature EJP frequency compared to controls. The mEJP amplitude is increased, similar to that seen in Blos1^EY06269/+ mutant flies.

One copy of Dysb^e01028 suppresses the dominant changes in mEJP amplitude and quantal content seen in Blos1^ex65/+ mutant NMJs. The increase in bouton number seen in Blos1^ex65/+ NMJs is also suppressed. Dysb^e01028 Blos1^ex65 double heterozygotes exhibit deficits in short term olfactory habituation. This phenotype is not observed in either heterozygote alone.

Dysb^e01028 Blos1^ex2 double heterozygotes exhibit deficits in short term olfactory habituation. This phenotype is not observed in either heterozygote alone.

(Mullin et al., 2015)

Dysb^e01028 heterozygotes that are also heterozygous for Df(2L)Exel6277 (which removes the entire Snapin locus), exhibit significantly less homeostatic compensation compared with either heterozygous mutant alone. Co-expression of Snapin^Scer\UAS.cDa in motorneurons (under the control of Scer\GAL4^VGlut-OK371) restores homeostasis towards control levels (although this rescue is not complete).

Double-heterozygous Syt1^AD4/+ ; Dysb^e01028/+ flies exhibit normal homeostatic compensation.

(Dickman et al., 2012)

e¹/dysb^e01028 heteroallelic mutants display locomotor hyperactivity and mating disorientation (loss of the strong male bias towards the courtship of females).

(Shao et al., 2011)

GluRIIA^SP16 ; dysb^e01028 double mutant larvae do not show homeostatic compensation at the neuromuscular junction.

The phenotype of reduced synaptic homeostasis at the neuromuscular junction after treatment with philanthotoxin-433 that is seen in cac^S/+ larvae is not enhanced by dysb^e01028/+.

Expression of cac^{Scer\UAS.T:Avic\GFP-EGFP} under the control of Scer\GAL4^elav-C155 does not restore homeostatic compensation at the neuromuscular junction in dysb^e01028 larvae.

(Dickman and Davis, 2009)

Xenogenetic Interactions

Statement

Reference

The neuromuscular junction bouton phenotype characteristic for third instar larvae expressing Hsap\DISC1^{Scer\UAS.T:Ivir\HA1} under the control of Scer\GAL4^tub.PU is enhanced by combination with a single copy of the Dysb^e01028 allele: not only is the total bouton areas decreased further, in addition the total number of boutons as well as their individual size is significantly reduced compared to wild-type, whereas the number of axonal branching points remains normal.

(Furukubo-Tokunaga et al., 2016)

Pan-neuronal expression of Hsap\DTNBP1^Scer\UAS.cSa under the control of Scer\GAL4^elav-C155 rescues the larval neuromuscular junction excitatory junctional current defects and the adult short term memory defects observed in dysb^e01028 mutants.

Expression of Hsap\DTNBP1^Scer\UAS.cSa in the glia under the control of Scer\GAL4^repo partially suppresses the locomotor defects seen in dysb^e01028 mutants. The increase in dopamine levels seen in dysb^e01028 mutant heads is also suppressed.

(Shao et al., 2011)

Complementation and Rescue Data

Rescued by

Dysb[+]/Dysb^e01028 is rescued by Scer\GAL4^elav-C155/Dysb^UAS.Venus

(Gokhale et al., 2016)

Dysb^e01028 is rescued by Dysb^UAS.cSa/Scer\GAL4^VGlut1-OK371

(Shao et al., 2011)

Dysb^e01028 is rescued by Dysb^UAS.cSa/Scer\GAL4^hs.PU

(Shao et al., 2011)

Dysb^e01028 is rescued by Dysb^UAS.Venus/Scer\GAL4^elav-C155

(Dickman and Davis, 2009)

Partially rescued by

Dysb^e01028 is partially rescued by Dysb^UAS.Venus/Scer\GAL4^RapGAP1-OK6

(Chen et al., 2017)

Dysb^e01028 is partially rescued by Scer\GAL4^elav-C155/Dysb^UAS.cSa

(Shao et al., 2011)

Dysb^e01028 is partially rescued by Dysb^UAS.cSa/Scer\GAL4^repo

(Shao et al., 2011)

Not rescued by

Dysb^e01028 is not rescued by Scer\GAL4^Mhc.PW/Dysb^UAS.cDa

(Dickman and Davis, 2009)

Comments

The expression of Dysb^{Scer\UAS.T:Avic\GFP-YFP.Venus} under the control of Scer\GAL4^RapGAP1-OK6 partially suppresses both the increased rate of depletion and the decreased rate of recovery of the synaptic vesicle pool upon high-frequency stimulation of the neuromuscular junction exhibited by Dysb^e01028 homozygous wandering third instar larvae.

(Chen et al., 2017)

The increased number of boutons on neuromuscular junctions observed in Dysb^e01028/+ heterozygous third instar larvae is suppressed by expression of Dysb^{Scer\UAS.T:Avic\GFP-YFP.Venus} under the control of Scer\GAL4^elav-C155 in the mutant background.

(Gokhale et al., 2016)

Presynaptic expression of Dysb^Scer\UAS.cDa using Scer\GAL4^elav-C155 restores the homeostatic quantal content increase to wild-type levels in Dysb^e01028 mutants.

(Gokhale et al., 2015)

Expression of dysb^Scer\UAS.cSa under the control of Scer\GAL4^elav-C155 rescues the attenuated excitatory junctional currents recorded in the larval neuromuscular junction in dysb^e01028 mutants. The short term memory defects are also rescued. The locomotor and mating disorientation phenotypes are not rescued, nor is the dopamine level in dysb^e01028 mutant heads.

Expression of dysb^Scer\UAS.cSa in glia under the control of Scer\GAL4^repo fails to rescue the short term memory defects seen in dysb^e01028 mutant flies. However, glial expression of dysb^Scer\UAS.cSa is able to rescue the locomotor and mating disorientation phenotypes. The increased dopamine levels in the head are also rescued.

Expression of dysb^Scer\UAS.cSa in glutamatergic neurons under the control of Scer\GAL4^VGlut-OK371 rescues the short-term memory defects seen in dysb^e01028 mutant flies.

Acute expression of dysb^Scer\UAS.cSa under the control of Scer\GAL4^hs.PU rescues the short-term memory defects and mating disorientation seen in dysb^e01028 mutant flies. The increase in dopamine levels seen in dysb^e01028 mutant heads is also suppressed.

(Shao et al., 2011)

Images (0)

Mutant

Wild-type

Stocks (1)

Bloomington

17918

w¹¹¹⁸; PBac{RB}Dysb^e01028/TM6B, Tb¹

Notes on Origin

Discoverer

External Crossreferences and Linkouts ( 0 )

Synonyms and Secondary IDs (10)

Reported As

Symbol Synonym

CG6856^e01028

Dysb^e01028

dysb1

(Gokhale et al., 2015, Gokhale et al., 2015)

dysb¹

(Baccino-Calace et al., 2022, Hidalgo et al., 2020, Chen et al., 2017, Gokhale et al., 2016, Gokhale et al., 2015, Mullin et al., 2015, Lu et al., 2014, Dickman et al., 2012, Shao et al., 2011, Dickman and Davis, 2009)

dysb^1A

(Gokhale et al., 2015)

dysb^1a

(Gokhale et al., 2015)

dysb^e01028

(Furukubo-Tokunaga et al., 2016)

dysbindin¹

(Baccino-Calace et al., 2022)

dysbindin^e01028

(Chen et al., 2017)

pBac^e01028

(Shao et al., 2011)

Name Synonyms

Secondary FlyBase IDs

References (16)

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