FlyBase Allele Report: Dmel\Fas2[UAS.cLb]

General Information

Symbol

Dmel\Fas2^UAS.cLb

Species

D. melanogaster

Name

Saccharomyces cerevisiae UAS construct b of Lin

FlyBase ID

FBal0066094

Feature type

allele

Associated gene

Dmel\Fas2

Associated Insertion(s)

Carried in Construct

P{UAS-Fas2.PEST+}

Key Links

Transgenic product class

cDNA

(Lin, 1997.11.4)

wild_type

(Lin, 1997.11.4)

Mutagen

in vitro construct

Nature of the Allele

Transgenic product class

cDNA

(Lin, 1997.11.4)

wild_type

(Lin, 1997.11.4)

Mutagen

in vitro construct

(Davis et al., 1997)

Progenitor genotype

Carried in construct

P{UAS-Fas2.PEST+}

Cytology

Description

Expression of the PEST[+] transmembrane isoform of Fas2 is governed by UASt regulatory sequences.

(Davis et al., 1997)

Expression of a Fas2 PEST+ cDNA (with the ends of the cDNA modified to remove all 5' and 3' untranslated sequences) is governed by UASt regulatory sequences.

(Lin, 1997.11.4)

Allele components

Component

Use(s)

Regulatory region(s)

UASt

binary expression system - regulatory region

Encoded product / tool

Fas2

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 ( 0 )

Disease

Interaction

References

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

Disease-implicated variant(s)

Phenotypic Data

Phenotypic Class

abnormal neuroanatomy, with Scer\GAL4^B185

(Davis et al., 1997)

abnormal neuroanatomy, with Scer\GAL4^ChAT.7.4, Scer\GAL4^eve.RRK

(Baines et al., 2002)

abnormal neuroanatomy, with Scer\GAL4^elav.PLu

(Davis et al., 1997)

abnormal neuroanatomy, with Scer\GAL4^eve.RRK

(Baines et al., 2002)

abnormal neuroanatomy, with Scer\GAL4^how-24B

(Davis et al., 1997)

abnormal neuroanatomy, with Scer\GAL4^{l(2)E105-E105}

(Davis et al., 1997)

abnormal neuroanatomy, with Scer\GAL4^l(3)H94-H94

(Davis and Goodman, 1998, Davis et al., 1997)

abnormal neuroanatomy, with Scer\GAL4^Mhc.PW

(Davis et al., 1997)

abnormal neuroanatomy, with Scer\GAL4^MS1075

(Kristiansen et al., 2005)

abnormal neuroanatomy | somatic clone, with Scer\FLP1^UAS.cUa, Scer\GAL4^Act.PU, Scer\GAL4^eve.RRK

(Timmerman et al., 2013)

abnormal neurophysiology, with Scer\GAL4^ChAT.7.4

(Baines et al., 2002)

abnormal neurophysiology, with Scer\GAL4^eve.RRK

(Baines et al., 2002)

Phenotype Manifest In

bouton, with Scer\GAL4^B185

(Davis et al., 1997)

bouton, with Scer\GAL4^elav.PLu

(Davis et al., 1997)

bouton, with Scer\GAL4^how-24B

(Davis et al., 1997)

bouton, with Scer\GAL4^{l(2)E105-E105}

(Davis et al., 1997)

bouton, with Scer\GAL4^l(3)H94-H94

(Davis et al., 1997)

bouton, with Scer\GAL4^Mhc.PW

(Davis et al., 1997)

dendrite | somatic clone, with Scer\FLP1^UAS.cUa, Scer\GAL4^Act.PU, Scer\GAL4^eve.RRK

(Timmerman et al., 2013)

larval DA1 motor neuron, with Scer\GAL4^ChAT.7.4

(Baines et al., 2002)

larval RP2 motor neuron, with Scer\GAL4^ChAT.7.4

(Baines et al., 2002)

larval RP2 motor neuron | somatic clone, with Scer\FLP1^UAS.cUa, Scer\GAL4^Act.PU, Scer\GAL4^eve.RRK

(Timmerman et al., 2013)

larval RP5 motor neuron, with Scer\GAL4^l(3)H94-H94

(Davis and Goodman, 1998)

larval transverse nerve, with Scer\GAL4^l(3)H94-H94

(Winberg et al., 1998)

larval VL3/4 motor neuron, with Scer\GAL4^ChAT.7.4, Scer\GAL4^eve.RRK

(Baines et al., 2002)

larval VL3/4 motor neuron, with Scer\GAL4^l(3)H94-H94

(Davis and Goodman, 1998)

larval VO2 motor neuron, with Scer\GAL4^l(3)H94-H94

(Davis and Goodman, 1998)

mechanosensory neuron, with Scer\GAL4^MS1075

(Kristiansen et al., 2005)

ocellar nerve, with Scer\GAL4^MS1075

(Kristiansen et al., 2005)

synapse, with Scer\GAL4^ChAT.7.4, Scer\GAL4^eve.RRK

(Baines et al., 2002)

synapse, with Scer\GAL4^l(3)H94-H94

(Davis and Goodman, 1998)

synapse & aCC neuron, with Scer\GAL4^eve.RRK

(Baines et al., 2002)

synapse & RP2 neuron, with Scer\GAL4^eve.RRK

(Baines et al., 2002)

synapse | ectopic, with Scer\GAL4^B185

(Davis et al., 1997)

synapse | ectopic, with Scer\GAL4^elav.PLu

(Davis et al., 1997)

synapse | ectopic, with Scer\GAL4^how-24B

(Davis et al., 1997)

synapse | ectopic, with Scer\GAL4^{l(2)E105-E105}

(Davis et al., 1997)

synapse | ectopic, with Scer\GAL4^l(3)H94-H94

(Davis and Goodman, 1998, Davis et al., 1997)

synapse | ectopic, with Scer\GAL4^Mhc.PW

(Davis et al., 1997)

Detailed Description

Statement

Reference

Overexpression of Fas2^Scer\UAS.cLb driven by Scer\GAL4^Tab2-201Y does not affect axon pruning.

(Bornstein et al., 2015)

Expression of Fas2^Scer\UAS.cLb in the RP2 motor neurons (using the Scer\GAL4^eve.RRK driver to drive expression of Scer\FLP1^Scer\UAS.cUa which then induces clones of cells expressing Scer\GAL4^Act.PU) results in a decrease in dendritic complexity, number of dendritic branches and total dendrite length compared to controls.

(Timmerman et al., 2013)

Scer\GAL4^Rapgap1-OK6-mediated expression of Fas2^Scer\UAS.cLb has no effect on NMJ synaptic bouton number.

(Beck et al., 2012)

Scer\GAL4^MS1075-driven expression of Fas2^Scer\UAS.cLb causes only a sporadic phenotype (10% of heads analyzed at 29[o]C have some OP and 15% some BM axon alterations).

(Kristiansen et al., 2005)

Expression of Fas2^UAS.cLb in all neurons of the CNS (under the regulation of Scer\GAL4^insc-Mz1407) does not influence the frequency of synaptic inputs. However, selective expression of Fas2^UAS.cLb in either aCC/RP2 (Scer\GAL4^eve.RRK) or presynaptic cholinergic neurons (Scer\GAL4^ChAT.7.4) significantly reduces the input frequency. Simultaneous expression of Fas2^UAS.cLb in both presynaptic cholinergic neurons and aCC/RP2 (under the control of both Scer\GAL4^eve.RRK and Scer\GAL4^ChAT.7.4) does not influence the frequency of synaptic drive.

Expression of Fas2^UAS.cLb in aCC/RP2 (Scer\GAL4^eve.RRK) does not influence the frequency of suprathreshold synaptic drive in the RP3 motor neuron (which does not express GAL4 in these larvae). However, combined expression in both aCC/RP2 (Scer\GAL4^eve.RRK) and cholinergic interneurons (Scer\GAL4^ChAT.7.4) results in a significant decrease in the frequency of suprathreshold synaptic drive. The effect of expressing Fas2^UAS.cLb in aCC/RP2 (under the control of Scer\GAL4^eve.RRK) can be rescued by the presence of Scer\GAL80^eve.RRK in these motor neurons.

Ultrastructural analysis reveals that expression of Fas2^UAS.cLb in aCC (Scer\GAL4^eve.RRK) significantly reduces the number of presynaptic terminals observed to contact this neuron. Simultaneous expression of Fas2^UAS.cLb in both aCC (Scer\GAL4^eve.RRK) and cholinergic neurons (Scer\GAL4^ChAT.7.4) does not, however, affect the number of presynaptic terminals that contact aCC.

Expression of Fas2^UAS.cLb in aCC does not reduce the number of presynaptic terminals that contact RP3. Presynaptic terminals contacting this neuron (which does not express GAL4 in these larvae) are significantly reduced in number after the combined expression of Fas2^UAS.cLb in both aCC/RP2 (Scer\GAL4^eve.RRK) and cholinergic neurons (Scer\GAL4^ChAT.7.4).

Expressing Fas2^UAS.cLb in aCC/RP2 neurons through the control of Scer\GAL4^eve.RRK significantly reduces the frequency of suprathreshold inputs recorded in L1 (~4hrs after hatching at 25[o]C).

Recordings of synaptic transmission, under voltage clamp conditions(V[[h]] -60mV), show that when Fas2^UAS.cLb is expressed in aCC/RP2 (under the regulation of Scer\GAL4^eve.RRK), the amplitude distribution of evoked synaptic currents is significantly reduced compared with controls (GAL4-only/UAS-only lines).

Using Scer\GAL4^ChAT.7.4 to drive expression of Fas2^UAS.cLb in all cholinergic neurons results in a significant reduction in the frequency of suprathreshold synaptic drive recorded in aCC/RP2 neurons.

Expression of Fas2^UAS.cLb simultaneously in both cholinergic neurons (Scer\GAL4^ChAT.7.4) and in aCC/RP2 (Scer\GAL4^eve.RRK) does not result in a reduction in the frequency of suprathreshold synaptic inputs during L1 and does not affect the number of presynaptic terminals that contact aCC. In these experiments however, recordings from the RP3 motor neuron show a marked reduction in synaptic drive and in the number of presynaptic terminals that contact RP3.

Expression of Fas2^UAS.cLb in all neurons of the embryo (under the control of Scer\GAL4^insc-Mz1407) does not alter the frequency of suprathreshold synaptic currents recorded in aCC/RP2 in L1. The expression of Fas2 in these larvae does not, however, affect the number of presynaptic terminals that contact RP3.

(Baines et al., 2002)

Scer\GAL4^l(3)H94-H94-mediated expression on muscle 6 biases synapse formation and growth of neurons RP3 and 6/7 towards muscle 6 (total bouton number of these motor neurons does not change) and away from muscle 7. Overexpression also stabilises ectopic synapses on muscle 6 but not muscle 7. Ectopic synapses participate in muscle depolarisation. Muscle 6 becomes hyperinnervated receiving 91% more boutons than normal, muscle 7 receives 40% fewer boutons than normal. Muscle 13 also becomes hyperinnervated, receiving the majority of synapses from both motor neuron RP1 and RP5, receiving 162% more boutons than normal. Muscle 12 receives 34% fewer boutons. Muscles 7 and 12 exhibit a reduction in innervation by motor neurons RP3 and RP5, this is accompanied by a significant reduction in bouton number. Intracellular recording from the hyperinnervated muscles 6 and 13 during nerve stimulation shows muscle depolarisation is normal, quantal size is normal. The per-bouton probability of transmitter release is decreased at these superinnervated muscles. Scer\GAL4^Mhc.PW-mediated expression causes no change in the pattern of synaptic connections and number of synaptic boutons.

(Davis and Goodman, 1998)

Scer\GAL4^l(3)H94-H94-mediated expression causes ectopic transverse nerve contacts.

(Winberg et al., 1998)

A transient increase in muscle Fas2^Scer\UAS.cLb stabilizes growth cone contacts and leads to synapses that are functional and stable. Targets that normally receive two inputs can now receive up to six. Overexpression in the muscle stabilizes novel, ectopic synapses on all muscles examined in detail including muscles 6, 7, 12 13, 4, 3 and 2. Changing the relative levels of Fas2^Scer\UAS.cLb on neighboring muscles leads to dramatic shifts in target selection. Differential levels of Fas2 protein not only influence the stablization of novel synaptic connections but also appear to regulate the further growth of these synapses. The ectopic synapses caused by ectopic expression of Fas2^Scer\UAS.cLb are functional as assayed for EJPs.

(Davis et al., 1997)

External Data

Linkouts

Interactions

Show genetic interaction network for Enhancers & Suppressors

Phenotypic Class

Suppressor of

Statement

Reference

Fas2^UAS.cLb/Scer\GAL4^RapGAP1-OK6 is a suppressor of abnormal neuroanatomy | third instar larval stage phenotype of beag¹/Df(3R)Exel6151

(Beck et al., 2012)

Fas2^UAS.cLb/Scer\GAL4^RapGAP1-OK6 is a suppressor | partially of abnormal neuroanatomy | third instar larval stage phenotype of Smu1^f03090/Df(3R)Exel6182

(Beck et al., 2012)

Other

Statement

Reference

Fas2^UAS.cLb, Scer\GAL4^Tab2-201Y, bsk^DN.UAS.cUa has abnormal neuroanatomy phenotype

(Bornstein et al., 2015)

Phenotype Manifest In

Enhanced by

Statement

Reference

Fas2^UAS.cLb, Scer\GAL4^l(3)H94-H94 has larval transverse nerve phenotype, enhanceable by Sema2a⁰³⁴⁷⁴

(Winberg et al., 1998)

Suppressed by

Statement

Reference

Fas2^UAS.cLb, Scer\GAL4^l(3)H94-H94 has larval transverse nerve phenotype, suppressible by Sema2a^UAS.cKa, Scer\GAL4^l(3)H94-H94

(Winberg et al., 1998)

Suppressor of

Statement

Reference

Fas2^UAS.cLb/Scer\GAL4^RapGAP1-OK6 is a suppressor of NMJ bouton | third instar larval stage phenotype of beag¹/Df(3R)Exel6151

(Beck et al., 2012)

Fas2^UAS.cLb/Scer\GAL4^RapGAP1-OK6 is a suppressor | partially of NMJ bouton | third instar larval stage phenotype of Smu1^f03090/Df(3R)Exel6182

(Beck et al., 2012)

Other

Statement

Reference

Fas2^UAS.cLb, Scer\GAL4^Tab2-201Y, bsk^DN.UAS.cUa has axon phenotype

(Bornstein et al., 2015)

Additional Comments

Genetic Interactions

Statement

Reference

Co-expression of Fas2^Scer\UAS.cLa, Fas2^Scer\UAS.cLb or Fas2^C.Scer\UAS in third instar larvae with GluRIIC^{dsRNA.Scer\UAS.cBa} simultaneously driven by Scer\GAL4^C57 and Scer\GAL4^elav-C155 does not impair homeostatic compensation at the neuromuscular junction (significant reduction in mEPSP and significant increase in quantal content compared to controls, just as is seen in larvae with expression of GluRIIC^{dsRNA.Scer\UAS.cBa} simultaneously driven by Scer\GAL4^C57 and Scer\GAL4^elav-C155).

(Spring et al., 2016)

Co-expression of bsk^{DN.Scer\UAS.cUa} and Fas2^Scer\UAS.cLb by Scer\GAL4^Tab2-201Y results in mushroom body γ lobe axon pruning defects.

(Bornstein et al., 2015)

Scer\GAL4^Rapgap1-OK6-mediated expression of Fas2^Scer\UAS.cLb rescues synaptic bouton number and average synaptic bouton area of beag¹/Df(3R)Exel6151 animals to wild type.

Scer\GAL4^Rapgap1-OK6-mediated expression of Fas2^Scer\UAS.cLb partially rescues synaptic bouton number Smu1^f03090/Df(3R)Exel6182 animals.

(Beck et al., 2012)

Fas2^Scer\UAS.cLb overexpression under the control of Scer\GAL4^MS1075 can rescue the Nrg^l3 phenotype at the restrictive temperature, including OP axon alterations. In contrast, expression of Fas2^Scer\UAS.cLb in BM axons and the epidermis (under the control of Scer\GAL4^MS1075) does not rescue the Nrg^l3 BM axonal alterations, but rather enhances them synergistically.

(Kristiansen et al., 2005)

Ectopic transverse nerve contacts caused by expression of Fas2^Scer\UAS.cLb under the control of Scer\GAL4^l(3)H94-H94 is enhanced by loss of Sema-2a function (Sema-2a⁰³⁴⁷⁴) and suppressed by overexpression of Sema-2a (Sema-2a^Scer\UAS.cKa Scer\GAL4^l(3)H94-H94).

(Winberg et al., 1998)

Xenogenetic Interactions

Statement

Reference

Complementation and Rescue Data

Rescues

Fas2^UAS.cLb/Scer\GAL4^RapGAP1-OK6 rescues Df(1)BSC869/Fas2^e76

(Beck et al., 2012)

Comments

Scer\GAL4^Rapgap1-OK6-mediated expression of Fas2^Scer\UAS.cLb fully rescues the reduced bouton number of Fas2^e76/Df(1)BSC869 animals.

(Beck et al., 2012)

Images (0)

Mutant

Wild-type

Stocks (2)

Bloomington

606043

w¹¹¹⁸; P{UAS-Fas2^GPI.D}2, P{UAS-Fas2.PEST+}2; P{UAS-elff.G}1M0M/TM2

606044

w¹¹¹⁸; P{UAS-Fas2^GPI.D}2, P{UAS-Fas2.PEST+}2; P{UAS-fipi.G}3M1M/TM2

Notes on Origin

Discoverer

D. Lin.

(Davis et al., 1997)

External Crossreferences and Linkouts ( 0 )

Synonyms and Secondary IDs (3)

Reported As

Symbol Synonym

Fas2^Scer\UAS.cLb

Fas2^UAS.cLb

Name Synonyms

Saccharomyces cerevisiae UAS construct b of Lin

(Davis et al., 1997)

Secondary FlyBase IDs

References (15)

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