Allele Dmel\Fas2^Scer\UAS.cLb

General Information
Symbol	Dmel\Fas2^Scer\UAS.cLb	Species	D. melanogaster
Name	Saccharomyces cerevisiae UAS construct b of Lin	FlyBase ID	FBal0066094
Feature type	allele	Associated gene	Dmel\Fas2

Allele class
Mutagen	in vitro construct - regulatory fusion
Recent Updates
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FB2013_03
FB2013_02
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Nature of the Allele
Allele class
Mutagen	in vitro construct - regulatory fusion (Davis et al., 1997)
Mutations Mapped to the Genome

Type Location Additional Notes References
Associated Sequence Data
DDBJ / EMBL / GenBank	DNA sequence Protein sequence Name

UniProtKB/Swiss-Prot
UniProtKB/TrEMBL

Progenitor genotype
Nature of the lesion	Statement Reference Construct: Expression of a PEST⁺ transmembrane isoform of Fas2 is governed by Scer\UAS 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 Scer\UAS regulatory sequences. (Lin, 1997.11.4)
Carried in construct	P{UAS-Fas2.PEST+} (Davis and Goodman, 1998, Baines et al., 2002, Lin, 1997.11.4, Davis et al., 1997, Winberg et al., 1998, Kristiansen et al., 2005, Banovic et al., 2010, Beck et al., 2012, Mosca et al., 2012)
Cytology
Phenotypic Data
Phenotypic Class
	neuroanatomy defective, with Scer\GAL4^B19, Scer\GAL4^eve.RRK (Baines et al., 2002) neuroanatomy defective, with Scer\GAL4^B185 (Davis et al., 1997) neuroanatomy defective, with Scer\GAL4^elav.PLu (Davis et al., 1997) neuroanatomy defective, with Scer\GAL4^eve.RRK (Baines et al., 2002) neuroanatomy defective, with Scer\GAL4^how-24B (Davis et al., 1997) neuroanatomy defective, with Scer\GAL4^{l(2)E105-E105} (Davis et al., 1997) neuroanatomy defective, with Scer\GAL4^l(3)H94-H94 (Davis et al., 1997, Davis and Goodman, 1998) neuroanatomy defective, with Scer\GAL4^Mhc.PW (Davis et al., 1997) neuroanatomy defective, with Scer\GAL4^MS1075 (Kristiansen et al., 2005) neurophysiology defective, with Scer\GAL4^B19 (Baines et al., 2002) neurophysiology defective, 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) mechanosensory neuron, with Scer\GAL4^MS1075 (Kristiansen et al., 2005) ocellar nerve, with Scer\GAL4^MS1075 (Kristiansen et al., 2005) RP1 motor neuron, with Scer\GAL4^l(3)H94-H94 (Davis and Goodman, 1998) RP3 motor neuron, with Scer\GAL4^l(3)H94-H94 (Davis and Goodman, 1998) RP5 motor neuron, with Scer\GAL4^l(3)H94-H94 (Davis and Goodman, 1998) synapse, with Scer\GAL4^l(3)H94-H94 (Davis and Goodman, 1998) synapse & aCC neuron, with Scer\GAL4^B19 (Baines et al., 2002) synapse & aCC neuron, with Scer\GAL4^eve.RRK (Baines et al., 2002) synapse & RP2 neuron, with Scer\GAL4^B19 (Baines et al., 2002) synapse & RP2 neuron, with Scer\GAL4^eve.RRK (Baines et al., 2002) synapse & RP3 neuron, with Scer\GAL4^B19, 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 et al., 1997, Davis and Goodman, 1998) synapse \| ectopic, with Scer\GAL4^Mhc.PW (Davis et al., 1997) transverse nerve, with Scer\GAL4^l(3)H94-H94 (Winberg et al., 1998)
Detailed Description
	Statement Reference 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^Scer\UAS.cLb in all neurons of the CNS (under the regulation of Scer\GAL4¹⁴⁰⁷) does not influence the frequency of synaptic inputs. However, selective expression of Fas2^Scer\UAS.cLb in either aCC/RP2 (Scer\GAL4^eve.RRK) or presynaptic cholinergic neurons (Scer\GAL4^B19) significantly reduces the input frequency. Simultaneous expression of Fas2^Scer\UAS.cLb in both presynaptic cholinergic neurons and aCC/RP2 (under the control of both Scer\GAL4^eve.RRK and Scer\GAL4^B19) does not influence the frequency of synaptic drive. Expression of Fas2^Scer\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^B19) results in a significant decrease in the frequency of suprathreshold synaptic drive. The effect of expressing Fas2^Scer\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^Scer\UAS.cLb in aCC (Scer\GAL4^eve.RRK) significantly reduces the number of presynaptic terminals observed to contact this neuron. Simultaneous expression of Fas2^Scer\UAS.cLb in both aCC (Scer\GAL4^eve.RRK) and cholinergic neurons (Scer\GAL4^B19) does not, however, affect the number of presynaptic terminals that contact aCC. Expression of Fas2^Scer\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^Scer\UAS.cLb in both aCC/RP2 (Scer\GAL4^eve.RRK) and cholinergic neurons (Scer\GAL4^B19). Expressing Fas2^Scer\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^oC). Recordings of synaptic transmission, under voltage clamp conditions(V_h -60mV), show that when Fas2^Scer\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^B19 to drive expression of Fas2^Scer\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^Scer\UAS.cLb simultaneously in both cholinergic neurons (Scer\GAL4^B19) 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^Scer\UAS.cLb in all neurons of the embryo (under the control of Scer\GAL4¹⁴⁰⁷) 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 the genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Suppressor of
Statement Reference Fas2^Scer\UAS.cLb/Scer\GAL4^Rapgap1-OK6 is a suppressor \| partially of neuroanatomy defective \| third instar larval stage phenotype of Smu1^f03090/Df(3R)Exel6182 (Beck et al., 2012) Fas2^Scer\UAS.cLb/Scer\GAL4^Rapgap1-OK6 is a suppressor of neuroanatomy defective \| third instar larval stage phenotype of beag¹/Df(3R)Exel6151 (Beck et al., 2012)
Phenotype Manifest In
Enhanced by
Statement Reference Fas2^Scer\UAS.cLb, Scer\GAL4^l(3)H94-H94 has transverse nerve phenotype, enhanceable by Sema-2a⁰³⁴⁷⁴ (Winberg et al., 1998)
Suppressed by
Statement Reference Fas2^Scer\UAS.cLb, Scer\GAL4^l(3)H94-H94 has transverse nerve phenotype, suppressible by Sema-2a^Scer\UAS.cKa, Scer\GAL4^l(3)H94-H94 (Winberg et al., 1998)
Suppressor of
Statement Reference Fas2^Scer\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) Fas2^Scer\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)
Additional Comments
Genetic Interactions
Statement Reference Scer\GAL4[Rapgap1-OK6]-mediated expression of Fas2[Scer\UAS.cLb] rescues synaptic bouton number and average synaptic bouton area of beag[1]/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 & Rescue Data
Rescues	Fas2^Scer\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)
Stocks ( 0 )

Notes on Origin
Discoverer	D. Lin.

External Crossreferences & Linkouts
Other Crossreferences

Linkouts

Synonyms & Secondary IDs ( 3 )
Reported As
Symbol Synonym	Fas2^Scer\UAS.cLb Fas2^UAS.cLb
Name Synonym	Saccharomyces cerevisiae UAS construct b of Lin (Davis et al., 1997)
Secondary FlyBase IDs

References ( 9 )
Research paper	Beck et al., 2012, J. Neurosci. 32(20): 7058--7073 Regulation of Fasciclin II and Synaptic Terminal Development by the Splicing Factor Beag. [FBrf0218385] Banovic et al., 2010, Neuron 66(5): 724--738 Drosophila Neuroligin 1 Promotes Growth and Postsynaptic Differentiation at Glutamatergic Neuromuscular Junctions. [FBrf0211035] Kristiansen et al., 2005, Mol. Cell. Neurosci. 28(1): 141--152 Genetic analysis of an overlapping functional requirement for L1- and NCAM-type proteins during sensory axon guidance in Drosophila. [FBrf0184161] Baines et al., 2002, J. Neurosci. 22(15): 6587--6595 Regulation of synaptic connectivity: levels of Fasciclin II influence synaptic growth in the Drosophila CNS. [FBrf0151382] Davis and Goodman, 1998, Nature 392(6671): 82--86 Synapse-specific control of synaptic efficacy at the terminals of a single neuron. [FBrf0100746] Winberg et al., 1998, Cell 93(4): 581--591 Genetic analysis of the mechanisms controlling target selection: complementary and combinatorial functions of netrins, semaphorins, and IgCAMs. [FBrf0102605] Davis et al., 1997, Neuron 19(3): 561--573 Genetic analysis of the mechanisms controlling target selection: target-derived Fasciclin II regulates the pattern of synapse formation. [FBrf0098766]
Supplementary material	Mosca et al., 2012, Nature 484(7393): Online methods. [FBrf0219881]
Personal communication to FlyBase	Lin, 1997.11.4, UAS-Fas2 and UAS-lacZ. UAS-Fas2 and UAS-lacZ. [FBrf0099039]

Allele Dmel\Fas2Scer\UAS.cLb

Allele Dmel\Fas2^Scer\UAS.cLb