|Name||Saccharomyces cerevisiae UAS construct b of Lin||FlyBase ID||FBal0066094|
|Feature type||allele||Associated gene||Dmel\Fas2|
|Mutagen||in vitro construct - regulatory fusion|
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|Nature of the Allele|
|Mutations Mapped to the Genome|
|Associated Sequence Data|
|Nature of the lesion|
Construct: Expression of a PEST+ transmembrane isoform of Fas2 is governed by Scer\UAS regulatory sequences.
|Carried in construct|
|Phenotype Manifest In|
Scer\GAL4[Rapgap1-OK6]-mediated expression of Fas2[Scer\UAS.cLb] has no effect on NMJ synaptic bouton number.
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).
Expression of Fas2Scer\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 Fas2Scer\UAS.cLb in either aCC/RP2 (Scer\GAL4eve.RRK) or presynaptic cholinergic neurons (Scer\GAL4B19) significantly reduces the input frequency. Simultaneous expression of Fas2Scer\UAS.cLb in both presynaptic cholinergic neurons and aCC/RP2 (under the control of both Scer\GAL4eve.RRK and Scer\GAL4B19) does not influence the frequency of synaptic drive. Expression of Fas2Scer\UAS.cLb in aCC/RP2 (Scer\GAL4eve.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\GAL4eve.RRK) and cholinergic interneurons (Scer\GAL4B19) results in a significant decrease in the frequency of suprathreshold synaptic drive. The effect of expressing Fas2Scer\UAS.cLb in aCC/RP2 (under the control of Scer\GAL4eve.RRK) can be rescued by the presence of Scer\GAL80eve.RRK in these motor neurons. Ultrastructural analysis reveals that expression of Fas2Scer\UAS.cLb in aCC (Scer\GAL4eve.RRK) significantly reduces the number of presynaptic terminals observed to contact this neuron. Simultaneous expression of Fas2Scer\UAS.cLb in both aCC (Scer\GAL4eve.RRK) and cholinergic neurons (Scer\GAL4B19) does not, however, affect the number of presynaptic terminals that contact aCC. Expression of Fas2Scer\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 Fas2Scer\UAS.cLb in both aCC/RP2 (Scer\GAL4eve.RRK) and cholinergic neurons (Scer\GAL4B19). Expressing Fas2Scer\UAS.cLb in aCC/RP2 neurons through the control of Scer\GAL4eve.RRK significantly reduces the frequency of suprathreshold inputs recorded in L1 (~4hrs after hatching at 25oC). Recordings of synaptic transmission, under voltage clamp conditions(Vh -60mV), show that when Fas2Scer\UAS.cLb is expressed in aCC/RP2 (under the regulation of Scer\GAL4eve.RRK), the amplitude distribution of evoked synaptic currents is significantly reduced compared with controls (GAL4-only/UAS-only lines). Using Scer\GAL4B19 to drive expression of Fas2Scer\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 Fas2Scer\UAS.cLb simultaneously in both cholinergic neurons (Scer\GAL4B19) and in aCC/RP2 (Scer\GAL4eve.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 Fas2Scer\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.
Scer\GAL4l(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\GAL4Mhc.PW-mediated expression causes no change in the pattern of synaptic connections and number of synaptic boutons.
Scer\GAL4l(3)H94-H94-mediated expression causes ectopic transverse nerve contacts.
A transient increase in muscle Fas2Scer\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 Fas2Scer\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 Fas2Scer\UAS.cLb are functional as assayed for EJPs.
Fas2Scer\UAS.cLb/Scer\GAL4Rapgap1-OK6 is a suppressor | partially of neuroanatomy defective | third instar larval stage phenotype of Smu1f03090/Df(3R)Exel6182
|Phenotype Manifest In|
Fas2Scer\UAS.cLb/Scer\GAL4Rapgap1-OK6 is a suppressor | partially of NMJ bouton | third instar larval stage phenotype of Smu1f03090/Df(3R)Exel6182
Scer\GAL4[Rapgap1-OK6]-mediated expression of Fas2[Scer\UAS.cLb] rescues synaptic bouton number and average synaptic bouton area of beag/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.
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.
|Complementation & Rescue Data|
|Stocks ( 0 )|
|Notes on Origin|
|External Crossreferences & Linkouts|
|Synonyms & Secondary IDs ( 3 )|
Saccharomyces cerevisiae UAS construct b of Lin
|Secondary FlyBase IDs|
|References ( 9 )|
|Personal communication to FlyBase|