FlyBase Allele Report: Dmel\PlexB[KG00878]

General Information

Symbol

Dmel\PlexB^KG00878

Species

D. melanogaster

Name

FlyBase ID

FBal0216740

Feature type

allele

Associated gene

Dmel\PlexB

Associated Insertion(s)

P{SUPor-P}PlexB^KG00878

Carried in Construct

Key Links

Genomic Maps

JBrowse

Allele class

Mutagen

Nature of the Allele

Allele class

Mutagen

Progenitor genotype

Associated Insertion(s)

P{SUPor-P}PlexB^KG00878

Cytology

Description

P{SUPor-P}PlexB^KG00878 is inserted approximately 70bp after the start codon.

(Bates and Whitington, 2007)

Allele components

Component

Use(s)

Inserted element

P{SUPor-P}

insertional mutagenesis tool

Mutations Mapped to the Genome

Curation Data

Type

Location

Additional Notes

References

transposable_element_insertion_site

4:43,735..43,735 [+]

(Xie et al., 2019, Li et al., 2018, Hernandez-Fleming et al., 2017, Joo et al., 2013, Sweeney et al., 2011, FlyBase Curators, 2008-, Bates and Whitington, 2007, Ayoob et al., 2006)

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

ameliorates Charcot-Marie-Tooth disease type 2D

modeled by GlyRS^P234KY-2.UAS

(Grice et al., 2018)

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

Disease-implicated variant(s)

Phenotypic Data

Phenotypic Class

Phenotype Manifest In

adult olfactory receptor neuron

(Joo et al., 2013)

adult protocerebral bridge 1 glomerulus-fan-shaped body-round body type a neuron

(Xie et al., 2019)

dendrite | third instar larval stage

(Meltzer et al., 2016)

ellipsoid body

(Xie et al., 2019)

fan-shaped body

(Xie et al., 2019)

intermediate longitudinal fascicle | embryonic stage

(Wu et al., 2011)

larval intersegmental nerve

(Ayoob et al., 2006)

larval intersegmental nerve (with Df(4)M101-62f)

(Ayoob et al., 2006)

larval intersegmental nerve branch ISNb of A1-7 | embryonic stage

(Roh et al., 2016, Cho et al., 2012)

larval multidendritic class IV neuron | third instar larval stage

(Meltzer et al., 2016)

larval segmental nerve branch SNa of A1-7

(Ayoob et al., 2006)

larval segmental nerve branch SNa of A1-7 (with Df(4)M101-62f)

(Ayoob et al., 2006)

larval segmental nerve branch SNa of A1-7 | embryonic stage

(Roh et al., 2016, Cho et al., 2012)

lch1 neuron

(Bates and Whitington, 2007)

medial longitudinal fascicle

(Ayoob et al., 2006)

medial longitudinal fascicle (with Df(4)M101-62f)

(Ayoob et al., 2006)

MP1 tract

(Wu et al., 2011)

neuron projection | adult stage

(Xie et al., 2019)

Detailed Description

Statement

Reference

The adult brain of PlexB^KG00878 homozygotes exhibit defects in fan-shaped body (FB) and ellipsoid body (EB) morphology and P-Fr neurons innervated FB layer 6 and EB different than controls.

(Xie et al., 2019)

PlexB^KG00878 mutant larvae display increased dendritic non-contacting crossing in the class IV dendritic arborizing (da) neurons.

(Meltzer et al., 2016)

PlexB^KG00878 homozygous mutant embryos show ISNb axons presenting defasciculation defects at muscle 12 and innervation defects at muscles 6/7, but not ectopic innervations, as compared to controls; furthermore, their SNa axons frequently fail to innervate muscle 24, resulting in a 'stall' phenotype, and frequently show a double turn phenotype, as compared to controls.

(Roh et al., 2016)

In plexB^KG00878 mutant pupae, the dorsolateral axon trajectory is enlarged at the expense of the ventromedial trajectory. Adult plexB^KG00878 mutants also exhibit class-specific glomerular targeting defects, with ventromedial ORN classes displaying severe defects in both trajectory and target choice. While dorsolateral classes are unaffected, dorsomedial classes exhibit severe trajectory-choice defects but largely normal target selection.

(Joo et al., 2013)

Homozygous embryos show ISNb motor axon guidance defects (53.3% of hemisegments) and SNa motor axon guidance defects (32.5% of hemisegments).

(Cho et al., 2012)

The MP1 pathway is often disorganised, defasciculated and discontinuous in homozygous embryos.

(Wu et al., 2011)

The intermediate Fas2-positive longitudinal tract is severely disorganised in homozygous embryos, with phenotypes including defasciculation, disorganisation and wandering of axon bundles within this intermediate position. 71.0% of hemisegments show disorganisation of the intermediate Fas2-positive longitudinal tract. The medial and lateral Fas2-positive tracts appear normal in the mutant embryos.

Chordotonal organ axons extend into the central nervous system but fail to form regular terminal branches in the region of the disrupted intermediate longitudinal tract in mutant embryos, instead remaining stalled, with expanded, splayed out morphologies over the region where they would normally elaborate their synaptic contacts.

(Wu et al., 2011)

Stage 14 to 16 PlexB^KG00878 homozygous mutant embryos exhibit a v'ch1 axon mis-projection phenotype. In 14.7% of hemisegments the v'ch1 axon grows in an aberrant anterior direction to the cell bodies of lesA and/or 1daA, then mis-projects anteriorly to the ISN. These frequencies are significantly different from those observed in wild-type.

(Bates and Whitington, 2007)

plexB^KG00878 is semi-lethal and yields a small percentage (approximately 5.7%) of homozygous adult flies that are unable to mate successfully.

plexB^KG00878 homozygous embryos exhibit highly penetrant defects in axon guidance. Motor axons that contribute to the intersegmental nerve, the segmental nerve, and a subset of longitudinally projecting CNS axons, fail to defasciculate from one another.

plexB^KG00878 homozygous embryos do not exhibit defects in overall muscle morphology.

Motor axons in the Segmental nerve a (SNa) pathway are affected in plexB^KG00878 mutant embryos. In approximately almost 50% of all plexB^KG00878 hemisegments the anterior of the SNa dorsal branch incorrectly projects between muscles 21 and 22 instead of more posteriorly between muscles 22 and 23. In approximately 33.1% of all hemisegments the anteriorly misprojecting SNa motor axons take the wrong path but subsequently make two turns to reach their proper target. In approximately 14.7% of all plexB^KG00878 hemisegments the anteriorly projecting SNa dorsal branch takes the wrong path and is unable to reach its proper target.

plexB^KG00878 homozygous embryos exhibit defects in the innervation of the ventral muscles in most of the segments examined.

The medial Fas2-stained longitudinal fascicle in plexB^KG00878 mutants is severely defasciculated along its length.

plexB^KG00878/Df(4)M101-62f double heterozygous embryos exhibit phenotypes that are virtually identical to those observed in homozygous plexB^KG00878 embryos.

(Ayoob et al., 2006)

External Data

Linkouts

Interactions

Show genetic interaction network for Enhancers & Suppressors

Phenotypic Class

Enhanced by

Statement

Reference

PlexB^KG00878 has abnormal neuroanatomy | third instar larval stage phenotype, enhanceable by Df(2R)Sema2b-C4

(Meltzer et al., 2016)

PlexB^KG00878 has abnormal neuroanatomy phenotype, enhanceable by Sema2a⁰³⁰²¹

(Bates and Whitington, 2007)

PlexB^KG00878 has abnormal neuroanatomy phenotype, enhanceable by Df(4)C3

(Bates and Whitington, 2007)

NOT Enhanced by

Statement

Reference

PlexB^KG00878 has abnormal neuroanatomy | embryonic stage phenotype, non-enhanceable by Df(2R)B65/Df(2R)B65

(Roh et al., 2016)

PlexB^KG00878 has abnormal neuroanatomy | embryonic stage phenotype, non-enhanceable by Df(2R)Sema2b-C4/Df(2R)Sema2b-C4

(Roh et al., 2016)

PlexB^KG00878 has abnormal neuroanatomy | embryonic stage phenotype, non-enhanceable by Df(2R)A15/Df(2R)A15

(Roh et al., 2016)

Suppressed by

Statement

Reference

PlexB^KG00878 has abnormal neuroanatomy phenotype, suppressible by PlexA^UAS.Tag:HA/Scer\GAL4^elav-C155

(Ayoob et al., 2006)

PlexB^KG00878 has partially lethal - majority die phenotype, suppressible by PlexA^UAS.Tag:HA/Scer\GAL4^elav-C155

(Ayoob et al., 2006)

Enhancer of

Statement

Reference

PlexB^KG00878 is an enhancer of abnormal neuroanatomy phenotype of Sema2a⁰³⁴⁷⁴

(Bates and Whitington, 2007)

NOT Enhancer of

Statement

Reference

PlexB^KG00878/plexB[+] is a non-enhancer of abnormal neuroanatomy | embryonic stage phenotype of RhoGAPp190^RNAi.N.UAS, Scer\GAL4^elav.PLu

(Jeong et al., 2012)

Suppressor of

Statement

Reference

PlexB^KG00878 is a suppressor of abnormal neuroanatomy phenotype of Scer\GAL4^how-24B, Sema2a^UAS.cKa

(Ayoob et al., 2006)

NOT Suppressor of

Statement

Reference

PlexB^KG00878/plexB[+] is a non-suppressor of abnormal neuroanatomy | embryonic stage phenotype of RhoGAPp190^RNAi.N.UAS, Scer\GAL4^elav.PLu

(Jeong et al., 2012)

Phenotype Manifest In

Enhanced by

Statement

Reference

PlexB^KG00878 has larval multidendritic class IV neuron | third instar larval stage phenotype, enhanceable by Df(2R)Sema2b-C4

(Meltzer et al., 2016)

PlexB^KG00878 has dendrite | third instar larval stage phenotype, enhanceable by Df(2R)Sema2b-C4

(Meltzer et al., 2016)

PlexB^KG00878 has lch1 neuron phenotype, enhanceable by Sema2a⁰³⁰²¹

(Bates and Whitington, 2007)

NOT Enhanced by

Statement

Reference

PlexB^KG00878 has larval segmental nerve branch SNa of A1-7 | embryonic stage phenotype, non-enhanceable by Df(2R)B65/Df(2R)B65

(Roh et al., 2016)

PlexB^KG00878 has larval intersegmental nerve branch ISNb of A1-7 | embryonic stage phenotype, non-enhanceable by Df(2R)Sema2b-C4/Df(2R)Sema2b-C4

(Roh et al., 2016)

PlexB^KG00878 has larval segmental nerve branch SNa of A1-7 | embryonic stage phenotype, non-enhanceable by Df(2R)Sema2b-C4/Df(2R)Sema2b-C4

(Roh et al., 2016)

PlexB^KG00878 has larval intersegmental nerve branch ISNb of A1-7 | embryonic stage phenotype, non-enhanceable by Df(2R)A15/Df(2R)A15

(Roh et al., 2016)

PlexB^KG00878 has larval segmental nerve branch SNa of A1-7 | embryonic stage phenotype, non-enhanceable by Df(2R)A15/Df(2R)A15

(Roh et al., 2016)

PlexB^KG00878 has larval intersegmental nerve branch ISNb of A1-7 | embryonic stage phenotype, non-enhanceable by Df(2R)B65/Df(2R)B65

(Roh et al., 2016)

Suppressed by

Statement

Reference

PlexB^KG00878 has larval intersegmental nerve phenotype, suppressible by PlexA^UAS.Tag:HA/Scer\GAL4^elav-C155

(Ayoob et al., 2006)

PlexB^KG00878 has larval segmental nerve branch SNa of A1-7 phenotype, suppressible by PlexA^UAS.Tag:HA/Scer\GAL4^elav-C155

(Ayoob et al., 2006)

PlexB^KG00878 has medial longitudinal fascicle phenotype, suppressible by PlexA^UAS.Tag:HA/Scer\GAL4^elav-C155

(Ayoob et al., 2006)

Enhancer of

Statement

Reference

PlexB^KG00878 is an enhancer of lch1 neuron phenotype of Sema2a⁰³⁰²¹

(Bates and Whitington, 2007)

PlexB^KG00878 is an enhancer of lch1 neuron phenotype of Sema2a⁰³⁴⁷⁴

(Bates and Whitington, 2007)

NOT Enhancer of

Statement

Reference

PlexB^KG00878/plexB[+] is a non-enhancer of larval intersegmental nerve branch ISNb of A1-7 phenotype of RhoGAPp190^RNAi.N.UAS, Scer\GAL4^elav.PLu

(Jeong et al., 2012)

Suppressor of

Statement

Reference

PlexB^KG00878 is a suppressor of larval transverse nerve phenotype of Scer\GAL4^how-24B, Sema2a^UAS.cKa

(Ayoob et al., 2006)

NOT Suppressor of

Statement

Reference

PlexB^KG00878/plexB[+] is a non-suppressor of larval intersegmental nerve branch ISNb of A1-7 phenotype of RhoGAPp190^RNAi.N.UAS, Scer\GAL4^elav.PLu

(Jeong et al., 2012)

Additional Comments

Genetic Interactions

Statement

Reference

The level of non-contacting dendrite crossing in class IV dendrite arborizing larval neurons is significantly increased in PlexB^KG00878;Df(2R)Sema-2b-C4 double mutants compared to either PlexB^KG00878/+ or Df(2R)Sema-2b-C4/+ heterozygotes.

(Meltzer et al., 2016)

PlexB^KG00878, Df(2R)B65 double homozygous embryos, PlexB^KG00878, Df(2R)Sema2b-C4 double homozygous embryos or PlexB^KG00878, Df(2R)A15 double homozygous embryos show ISNb axon pathfinding defects which are similar to the defects observed in PlexB^KG00878 homozygotes rather than the more severe defects observed in Df(2R)B65, Df(2R)Sema2b-C4 or Df(2R)A15 homozygotes, respectively. Likewise, their SNa /guidance defects are similar to the defects observed in PlexB^KG00878 homozygotes rather than the less severe defects observed in Df(2R)B65, Df(2R)Sema2b-C4 or Df(2R)A15 homozygotes, respectively.

(Roh et al., 2016)

trol⁸/+ ; plexB^KG00878/+ double heterozygous embryo do not show significant ISNb or SNa motor axon guidance defects compared to controls.

(Cho et al., 2012)

Heterozygosity for plexB^KG00878 has no effect on the mutant ISNb phenotype seen in embryos expressing RhoGAPp190^{dsRNA.N.Scer\UAS} under the control of Scer\GAL4^elav.PLu.

(Jeong et al., 2012)

Sema-2a⁰³⁰²¹;;PlexB^KG00878 double homozygotes show v'ch1 mis-projections (27.8% of hemisegments) and lateral axon mis-projections (4.2% of hemisegments) at higher levels than in either single homozygous mutant.

In stage 14-16 Sema-2a⁰³⁴⁷⁴/+;; Df(4)C3/+ embryos, v'ch1 axon mis-projections to the intersegmental nerve are found in 3.7% of hemisegments, and 1ch5 mis-projections to the segmental nerve are found in 4.9% of hemisegments, which is significantly higher than that seen in either Sema-2a⁰³⁴⁷⁴ or Df(4)C3 heterozygotes alone.

(Bates and Whitington, 2007)

Expression of plexA^{Scer\UAS.T:Ivir\HA1} in a plexB^KG00878 mutant background rescues the total number of ISNb defasciculation defects by 25%, and the more severe ISNb bypass phenotypes by almost 50%. plexA^{Scer\UAS.T:Ivir\HA1} expression does not rescue the 'double turn' or 'lost' phenotypes of plexB^KG00878 mutants.

plexA^{Scer\UAS.T:Ivir\HA1} expression reduces the incidence of plexB^KG00878 SNa 'stall' phenotypes in plexB^KG00878 mutants by 20%. However, it does not reduce the total fraction of defective SNa pathways and is incapable of rescuing plexB^KG00878 CNS phenotypes.

Expression of plexA^{Scer\UAS.T:Ivir\HA1} also provides a modest reduction in the lethality observed in plexB^KG00878 mutants.

Approximately 58%of Df(3R)swp2^MICAL/+; plexB^KG00878/+ double transheterozygous embryonic hemisegments exhibit ISNb defects. This penetrance is equivalent to that seen for the same ISNb defects in plexB^KG00878 homozygous mutants.

A plexB^KG00878 background greatly reduces the tranverse nerve phenotype found in Sema-2a^Scer\UAS.cKa; Scer\GAL4^how-24B mutants (from aberrant formation in 27.9% to 12.2% of hemisegments).

(Ayoob et al., 2006)

Xenogenetic Interactions

Statement

Reference

Complementation and Rescue Data

Rescued by

PlexB^KG00878 is rescued by PlexB^UAS.cHa/Scer\GAL4^peb-GAL4

(Joo et al., 2013)

PlexB^KG00878 is rescued by Scer\GAL4^elav.PU/PlexB^UAS.Tag:MYC

(Wu et al., 2011)

PlexB^KG00878 is rescued by PlexB^UAS.cUa/Scer\GAL4^12.1

(Bates and Whitington, 2007)

PlexB^KG00878 is rescued by PlexB^UAS.cHa/Scer\GAL4^elav-C155

(Ayoob et al., 2006)

Partially rescued by

PlexB^KG00878/PlexB^{MI15559-TG4.1} is partially rescued by Scer\GAL4^{PlexB-MI15559-TG4.1}/PlexB^{EcTM.UAS.Tag:MYC}

(Xie et al., 2019)

PlexB^KG00878/PlexB^{MI15559-TG4.1} is partially rescued by Scer\GAL4^{PlexB-MI15559-TG4.1}/PlexB^UAS.cHa

(Xie et al., 2019)

PlexB^KG00878 is partially rescued by PlexB^UAS.cRa/Scer\GAL4^elav.PLu

(Roh et al., 2016)

Comments

Expression of either PlexB^UAS.cHa or PlexB^UAS.Tag:MYC under the control of Scer\GAL4^{PlexB-MI15559-TG4.1} almost completely rescues prior to eclosion lethality and partially rescues after eclosion lethality phenotypes of PlexB^KG00878/PlexB^{MI15559-TG4.1} transheterozygotes.

(Xie et al., 2019)

The ISNb and SNa axon pathfinding/guidance defects observed in homozygous PlexB^KG00878 mutant embryos are partially rescued by the expression of PlexB^UAS.cRa under the control of Scer\GAL4^elav.PLu.

(Roh et al., 2016)

Expression of PlexB^Scer\UAS.cUa in sensory neurons (under the control of Scer\GAL4^12.1) results in the frequency of the v'ch1 mis-projection phenotype decreasing from 14/7% to 4.8% in a PlexB^KG00878 background.

(Bates and Whitington, 2007)

plexB^KG00878 fails to complement Df(4)M101-62f with respect to the plexB^KG00878 lethality phenotype.

Expression of plexB^Scer\UAS.cHa in all neurons in a plexB^KG00878 homozygous background, under the control of Scer\GAL4^elav-C155, significantly rescues the intersegmental nerve b (ISNb) motor axon defects. Restoring plexB to all neurons also rescues the lethality associated with the plexB^KG00878 mutants (16.8% homozygous viable progeny compared to 5.7% of the plexB^KG00878/+ x Df(4)M101-62f/+ crossing being homozygous viable progeny).

Expression of plexB^Scer\UAS.cHa in all neurons in a plexB^KG00878 homozygous background, under the control of Scer\GAL4^elav-C155, significantly reduces the number of SNa defects by over 50%.

Expression of plexB^Scer\UAS.cHa in all neurons in a plexB^KG00878 homozygous background, under the control of Scer\GAL4^elav-C155 rescues the severe defasciculation of the medial Fas2-stained longitudinal fascicle.

(Ayoob et al., 2006)

Images (0)

Mutant

Wild-type

Stocks (1)

Bloomington

14579

y¹; ry⁵⁰⁶; P{SUPor-P}PlexB^KG00878/In(4)ci^D, ci^D pan^ciD

Notes on Origin

Discoverer

External Crossreferences and Linkouts ( 0 )

Synonyms and Secondary IDs (4)

Reported As

Symbol Synonym

PlexB^KG00878

(Xie et al., 2019, Roh et al., 2016, Zwarts et al., 2016, Cho et al., 2012, Jeong et al., 2012, Wu et al., 2011)

plexB^KG00878

(Guajardo et al., 2019, Grice et al., 2018, Li et al., 2018, Meltzer et al., 2016, Syed et al., 2016, Bates and Whitington, 2007, Ayoob et al., 2006)

plexB^KG878

(Shin and Diantonio, 2011)

plexinB^KG00878

(Hernandez-Fleming et al., 2017)

Name Synonyms

Secondary FlyBase IDs

References (20)

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