FlyBase Allele Report: Dmel\Syt1[AD4]

Syt1^AD4/Syt1^N13 transheterozygous larvae exhibit synaptic transmission defects across neuromuscular junctions, including severely defective synchronous neurotransmitter release, a large increase in failure rate following stimulation, and enhancement of the slower asynchronous phase of release. These defects are enhanced upon the expression of Syt1^{I426K.UAS.Tag:MYC} under the control of Scer\GAL4^elav-C155.

(Montes-Chinea et al., 2018)

Syt1^AD4 homozygotes are partially lethal and the rate of their lethality is further increased by Scer\GAL4^elav.PU-driven expression of Syt1^P-L.Scer\UAS and slightly reduced by expression of Syt1^Scer\UAS.cSb in the mutant background.

Syt1^AD4 heterozygotes expressing Syt1^P-L.Scer\UAS (with Scer\GAL4^elav.PU) have reduced adult lifespan (compared to flies expressing Syt1^Scer\UAS.cSb), at third instar larval stage the neural transmission at neuromuscular junction is impaired: the excitatory junction potential (EJP) amplitude is decreased but the amplitude as well as frequency of miniature EJP is unaffected as is the size of readily releasable pool of synaptic vesicles. However, the Syt1^P-L.Scer\UAS-expressing larvae also display significant decrease in the Ca[2+] affinity of release and larger paired pulse ratio, indicating a reduction in release probability, following either 10Hz or 50Hz train stimulation for 2sec, a significant decrease in synaptic depression is observed relative to controls but when a single stimulus is applied again 1 minute after the end of the stimulus train this effect is no longer evident. Syt1^AD4,Scer\GAL4^elav.PU/+;Syt1^P-L.Scer\UAS adults show reduced locomotor activity compared to age- and sex-matched controls but the circadian pattern of their activity is comparable to the Syt1^Scer\UAS.cSb-expressing controls, the mutants also show faster rate of muscle fatigue (measured in a modified climbing assay).

(Shields et al., 2017)

Nerve-evoked excitatory junction potentials (eEJPs) at third instar NMJs are absent in Syt1^N13/Syt1^AD4 mutants at either low (0.2mM) or high (1.0mM) external Ca[2+].

The frequency of spontaneous neurotransmitter release, as measured by mEJPs at third instar NMJs, is slightly but significantly increased in Syt1^N13/Syt1^AD4 mutants at low (0.2mM) external Ca[2+].

Scer\GAL4^elav-C155-mediated expression of Syt1^{C2A*-C2B*.Scer\UAS} in a Syt1^N13/Syt1^AD4 background results in spontaneous neurotransmitter release frequency (measured as mEJPs) at third instar NMJs far beyond the levels observed in controls.

Syt1^N13/Syt1^AD4 third instar larvae display a reduction in docked synaptic vesicles as well as a reduced vesicle density at type 1b boutons.

Scer\GAL4^elav-C155-mediated expression of Syt1^{C2B-C2B.Scer\UAS.T:Ivir\HA1} in a Syt1^N13/Syt1^AD4 background results in significantly enhanced spontaneous neurotransmitter release amplitude (measured as mEJPs) at third instar NMJs above the levels observed in controls.

(Lee et al., 2013)

Syt1^AD4 heterozygotes do not exhibit defects in synaptic homeostasis.

(Dickman et al., 2012)

Expression of Syt1^{D229E.Scer\UAS} under the control of Scer\GAL4^elav.PLu in a Syt1^AD4 mutant background (i.e. where there is no endogenous Syt1) decreases the synchronous evoked release by more than 80%. The mean amplitude of the EJP is markedly decreased in these mutants. However, spontaneous release is unchanged, both in amplitude and frequency. The evoked response is also significantly reduced compared to controls in extracellular Ca[2+] concentrations ranging from 0.6 to 5 mM. However, the apparent Ca[2+] affinity of release is decreased in Syt1^{D229E.Scer\UAS} flies; 45% more Ca[2+] is required to trigger a half maximal response, compared to controls. The Ca[2+] cooperativity of release is not affected in these flies.

(Striegel et al., 2012)

Syt1^N13/Syt1^AD4 hatching stage embryos lack the synchronous component of release when evoked release properties are recorded from muscle 6 following motor nerve stimulation in 4mM extracellular Ca[2+]. In contrast, a slower asynchronous release is uncovered. Total synaptic charge transfer following stimulation (reflecting the number of released vesicles) is reduced by 97.5% in the mutant synapses.

Expression of Syt1^{C2A-D3.4N.Scer\UAS} under the control of Scer\GAL4^elav.PLu in Syt1^N13/Syt1^AD4 embryos results in similar levels of evoked release and total charge transfer as wild-type controls when evoked release properties are recorded from muscle 6 following motor nerve stimulation in 4mM extracellular Ca[2+]. However, the asynchronous release seen in Syt1^N13/Syt1^AD4 embryos is even more prominent in Syt1^N13/Syt1^AD4 embryos expressing Syt1^{C2A-D3.4N.Scer\UAS} under the control of Scer\GAL4^elav.PLu. Syt1^N13/Syt1^AD4 embryos expressing Syt1^{C2A-D3.4N.Scer\UAS} under the control of Scer\GAL4^elav.PLu show an enhanced rate of spontaneous release compared to controls.

At lower Ca[2+] concentrations, recordings from muscle 6 following motor nerve stimulation in embryos expressing Syt1^{C2A-D3.4N.Scer\UAS} under the control of Scer\GAL4^elav.PLu in a Syt1^N13/Syt1^AD4 background have larger synaptic currents than controls, not only in the asynchronous component, but also in synchronous release.

Embryos expressing Syt1^{C2A-D3.4N.Scer\UAS} under the control of Scer\GAL4^elav.PLu in a Syt1^N13/Syt1^AD4 background show a similar level of hypertonic stimulated release as controls.

Expression of Syt1^{B-D3.4N.Scer\UAS} under the control of Scer\GAL4^elav.PLu largely suppresses the asynchronous component of release seen in Syt1^N13/Syt1^AD4 embryos when evoked release properties are recorded from muscle 6 following motor nerve stimulation in 4mM extracellular Ca[2+]. Only a small amount of residual synchronous release is seen in these embryos and the total charge transfer is dramatically reduced, similar to Syt1^N13/Syt1^AD4 embryos. Syt1^N13/Syt1^AD4 embryos expressing Syt1^{B-D3.4N.Scer\UAS} under the control of Scer\GAL4^elav.PLu show an enhanced rate of spontaneous release compared to controls.

Embryos expressing Syt1^{B-D3.4N.Scer\UAS} under the control of Scer\GAL4^elav.PLu in a Syt1^N13/Syt1^AD4 background show a similar level of hypertonic stimulated release as controls.

(Yoshihara et al., 2010)

Spontaneous miniature excitatory junction potential (mEJP) frequency at the neuromuscular junction is increased compared to controls in larvae expressing Syt1^KA.Scer\UAS under the control of Scer\GAL4^elav.PU in a Syt1^AD4 background. mEJP amplitude is normal. The mean amplitude, rise time, decay time, peak half width and area of the evoked EJP response are all normal in the mutant larvae. The number of synaptic vesicles is normal.

(Mace et al., 2009)

Evoked neurotransmitter release in Syt1^AD4/Syt1^N13 animals is characterized by a dramatic reduction in the overall number of vesicle fusion events, compared with controls, and a shift from fast fusion to a slower and prolonged asynchronous release of vesicles. Paired-pulse facilitation is enhanced compared with wild type across all extracellular Ca[2+] levels examined. Similar to wild type, the extent of facilitation in these mutants decreases with increasing interpulse interval. Syt1^AD4/Syt1^N13 mutants show a 5.6-fold reduction in the absolute number of vesicles released during the second pulse, compared with controls at identical extracellular Ca[2+].

(Saraswati et al., 2007)

syt^AD4 mutant synapses display two differences in terminal morphology compared with wild-type. Axons are thinner and more highly branched than controls. In addition, there are more satellite boutons protruding from the branches, with approximately 19.9 boutons per synapse compared to approximately 3.1 in wild-type.

(Dickman et al., 2006)

syt^AD4 photoreceptors form the correct number of synapses per presynaptic terminal independently of cartridge composition.

syt^AD4 mutants show a loss of synapses in photoreceptor neurons.

(Hiesinger et al., 2006)

Syt1^AD4/Syt1^D27 and Syt1^AD4/Syt1^N13 synapses show decreased evoked neurotransmitter release compared to wild-type controls. They also show a significantly slower time constant of endocytosis.

Syt1^AD4/Syt1^D27 and Syt1^AD4/Syt1^N13 synapses contain vesicles with a modest increase in diameter when at rest. After stimulation, there is a dramatic further increase in average vesicle diameter. Inspection of individual active zones demonstrates that vesicular structures with diameters greater than 10nm are observed throughout the vesicle cluster, both at the active zone and periactive zone region. The retrieval of abnormally large vesicles is on going at a time when most endocytosis has been completed in controls.

There is no difference in τ values in Syt1^AD4/Syt1^N13; Syt1^KQ.Scer\UAS Scer\GAL4^elav.PLu flies in response to a 50Hz, 10s stimulus, indicating that endocytosis rate is normal at Syt1^KQ.Scer\UAS synapses.

Syt1^AD4/Syt1^N13; Syt1^KQ.Scer\UAS Scer\GAL4^elav.PLu synapses at rest have a mean vesicle diameter equivalent to controls. Following stimulation, however, they show a significant further increase in mean vesicle diameter. Vesicles with diameters in excess of 80nm are observed.

Following a 50 Hz, 10 s stimulus, the peak ΔF/F SpH change in Syt1^AD4/Syt1^N13; Syt1^{B-D3.4N.Scer\UAS} Scer\GAL4^elav.PLuflies is reduced compared to controls, which agrees with prior electrophysiological demonstration of a decrease in evoked release. A slowed endocytosis rate constant is found at Syt1^{B-D3.4N.Scer\UAS} rescue synapses, with an average endocytic value that is more than 2-fold slower than controls. Increasing the Ca[2+] concentration speeds the rate of endocytosis, although not to control levels.

There is no difference in τ values in Syt1^AD4/Syt1^N13; Syt1^Scer\UAS.cMa Scer\GAL4^elav.PLu flies in response to a 50Hz, 10s stimulus.

There is no difference in the endocytic rate in Syt1^AD4/Syt1^N13; Syt1^{D229N.Scer\UAS} Scer\GAL4^elav.PLu flies compared to controls. There is also no change in mean vesicle diameter comparing rest and post-stimulation conditions.

(Poskanzer et al., 2006)

syt^AD4/syt^N13 null mutants exhibit dramatically slow larval locomotion. In addition to a decrease in distance travelled and locomotor cycle number, syt^AD4/syt^N13 mutants display an increase in the duration of a single locomotor cycle from 1 second to approximately 6 seconds. Synaptic transmission is severely decreased in syt^AD4/syt^N13 mutants, which show the characteristic slow rise and decay reflecting asynchronous release and a loss of the synchronous component of fusion.

(Adolfsen et al., 2004)

Larvae expressing syt^{B-D3.4N.Scer\UAS} under the control of Scer\GAL4^elav.PLu in a syt^AD4 background show a reduced mean excitatory junction potential (EJP) amplitude at the neuromuscular junction compared to syt^AD4 mutant larvae. The Ca²⁺ dependence of neurotransmitter release in larvae expressing syt^{B-D3.4N.Scer\UAS} under the control of Scer\GAL4^elav.PLu in a syt^AD4 background is significantly shifted compared to the Ca²⁺ dependence of neurotransmitter release in larvae expressing syt^Scer\UAS.cMa under the control of Scer\GAL4^elav.PLu in a syt^AD4 background.

(Mackler et al., 2002)

The excitatory junctional potential (EJP) amplitude at the neuromuscular junction is greatly reduced compared to wild type in syt^AD4/syt^D27 larvae. The EJP amplitude at the neuromuscular junction in homozygous larvae is 2.3 +/- 0.7mV compared to 41.1 +/- 0.7 mV in controls. There is a modest increase in frequency, but not amplitude, of spontaneous miniature EJPs.

(Robinson et al., 2002)

Synchronous release following stimulation of the neuromuscular junction is abolished in syt^AD4/syt^N13 mutants, with the appearance of residual delayed release that is not seen in controls. The population time constant for delayed release latencies is 115ms in the syt^AD4/syt^N13 mutants, compared to less than 6ms for synchronous release in wild type. Asynchronous release in syt^AD4/syt^N13 mutants shows a steep Ca²⁺ dependence. Release during repetitive stimulation at the syt^AD4/syt^N13 neuromuscular junction is asynchronous to nerve stimulation. The frequency of spontaneous miniature synaptic currents at the embryonic syt^AD4/syt^N13 neuromuscular junction is not increased compared to wild type. The quantal content of nerve evoked release at the neuromuscular junction is reduced in heterozygotes compared to controls.

(Yoshihara and Littleton, 2002)

Mutant synapses have significantly fewer SNARE complexes, as measured by reduction in hyperosmotic response at the embryonic synapse. Hyperosmotic response also shows increased latency.

(Fergestad et al., 2001)

If homozygous larvae are provided with a yeast solution, approximately 58% of first instar larvae survive to the third instar (if the yeast paste is too thick, the mutant larvae die). Approximately 92% of the surviving third instar larvae pupate, and in high humidity, approximately 59% of pupae eclose. Adults can survive for several days at 18^oC. although the majority die within 24 hours. When mutant larvae move, they are slow and quite uncoordinated. When mutant adult walk, they are extremely uncoordinated and fall often (some adults that land on their backs can right themselves, but with considerable difficulty). Mutant adults do not fly.

Mutants do not show any gross abnormalities in the growth of synaptic arborisations at the neuromuscular junction during larval development. Evoked neurotransmitter release at the neuromuscular junction is reduced by 94% in mutant larvae compared to wild type; the mean excitatory junctional potential (EJP) amplitude is 2.6 +/- 0.3 mV in mutant larvae (compared to 42.7 +/- 1.9 mV in controls). The evoked neurotransmitter release is asynchronous with the stimulus in the mutant larvae (but not in the wild-type controls). Spontaneous neurotransmitter release at the neuromuscular junction is increased in mutant larvae compared to wild type; the mean miniature EJP (mEJP) frequency is three-fold higher in mutant larvae (9.3 +/- 0.9 Hz) compared to controls (3.1 +/- 0.8 Hz).

(Loewen et al., 2001)

Viable, adult heterozygous flies containing a homozygous mutant eye (generated by mitotic recombination using the "EGUF/hid method") are recovered. The overall morphology of the eye and external morphology of the photoreceptors is normal. Electroretinograms do not have an on/off transient, indicating that phototransduction is normal but that synaptic transmission is defective.

(Stowers and Schwarz, 1999)

Homozygous and syt^AD4/syt^AD3 first larval instar nerve terminals contain fewer synaptic vesicles compared to wild-type and larger vesicles are more numerous in the mutant nerve terminals. The number of synaptic vesicles within 200nm of the presynaptic membrane is markedly reduced.

(Reist et al., 1998)

Sluggish and poorly coordinated movement. Some larvae hatch but do not show periodic peristaltic muscle contractions and die soon after hatching. Morphology of the neuromuscular junction of muscles 6 and 7 is normal suggesting a functional disruption.

(Broadie et al., 1994)

Many homozygous larvae hatch from the egg case (though well after the normal period) and show motor activity such as crawling and feeding. Transheterozygotes with Df(2L)DTD2 never survive to adulthood.

(DiAntonio and Schwarz, 1994)

Transheterozygote combinations with other syt alleles are lethal.

(Littleton et al., 1994)

Sluggish crawling and feeding behaviour. Larvae do not grow or moult as wild type larvae would, and die after a week (at 18^oC).

(DiAntonio et al., 1993)

External Data

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Interactions

Show genetic interaction network for Enhancers & Suppressors

Phenotypic Class

Enhanced by

Statement

Reference

Syt1^AD4/Syt1^N13 has increased mortality during development phenotype, enhanceable by Syt7^M1/Syt7^M1

(Guan et al., 2020)

Syt1^AD4/Syt1^N13 has abnormal neurophysiology | larval stage phenotype, enhanceable by Syt7^M1/Syt7^M1

(Guan et al., 2020)

NOT Enhanced by

Statement

Reference

Syt1^AD4/Syt1^N13 has abnormal neurophysiology phenotype, non-enhanceable by Syt4^BA1

(Saraswati et al., 2007)

Syt1^AD4/Syt1^N13 has uncoordinated phenotype, non-enhanceable by Scer\GAL4^elav-C155/Syt7^RNAi.UAS

(Saraswati et al., 2007)

Suppressed by

Statement

Reference

Syt1^AD4 has abnormal neurophysiology phenotype, suppressible by Syt4^UAS.cLa/Scer\GAL4^elav.PLu

(Robinson et al., 2002)

NOT suppressed by

Statement

Reference

Syt1^AD4/Syt1^N13 has lethal | third instar larval stage phenotype, non-suppressible by Syt7^UAS.cAa/Scer\GAL4^elav-C155

(Adolfsen et al., 2004)

Syt1^AD4/Syt1^N13 has lethal | third instar larval stage phenotype, non-suppressible by Scer\GAL4^elav-C155/Syt4^UAS.cLa

(Adolfsen et al., 2004)

Syt1^AD4/Syt1^N13 has lethal | third instar larval stage phenotype, non-suppressible by Scer\GAL4^elav-C155/Syt4^UAS.cLa/Scer\GAL4^elav.PLu

(Adolfsen et al., 2004)

Syt1^AD4/Syt1^N13 has abnormal locomotor rhythm | larval stage phenotype, non-suppressible by Scer\GAL4^elav-C155/Syt4^UAS.cLa

(Adolfsen et al., 2004)

Syt1^AD4/Syt1^N13 has abnormal locomotor rhythm | larval stage phenotype, non-suppressible by Scer\GAL4^elav-C155/Syt4^UAS.cLa/Scer\GAL4^elav.PLu

(Adolfsen et al., 2004)

Syt1^AD4/Syt1^N13 has abnormal neurophysiology phenotype, non-suppressible by Syt7^UAS.cAa/Scer\GAL4^elav-C155

(Adolfsen et al., 2004)

Syt1^AD4/Syt1^N13 has abnormal neurophysiology phenotype, non-suppressible by Scer\GAL4^elav-C155/Syt4^UAS.cLa

(Adolfsen et al., 2004)

Syt1^AD4/Syt1^N13 has abnormal neurophysiology phenotype, non-suppressible by Scer\GAL4^elav-C155/Syt4^UAS.cLa/Scer\GAL4^elav.PLu

(Adolfsen et al., 2004)

Syt1^AD4/Syt1^N13 has abnormal locomotor rhythm | larval stage phenotype, non-suppressible by Syt7^UAS.cAa/Scer\GAL4^elav-C155

(Adolfsen et al., 2004)

Suppressor of

Statement

Reference

(Tsai et al., 2019)

(Tsai et al., 2019)

Other

Statement

Reference

Scer\GAL4^elav-C155, Syt1^AD4/Syt1^N13, Syt7^RNAi.UAS has lethal | third instar larval stage phenotype

(Saraswati et al., 2007)

Syt1^D27/Syt1^AD4, Syt1^elav.PD, stnA¹⁵, stnB¹⁵ has viable phenotype

(Phillips et al., 2000)

Syt1^D27/Syt1^AD4, Syt1^elav.PD, stnA⁶ has lethal phenotype

(Phillips et al., 2000)

Syt1^D27/Syt1^AD4, Syt1^elav.PD, stnA⁶ has uncoordinated phenotype

(Phillips et al., 2000)

Syt1^D27/Syt1^AD4, Syt1^elav.PD, stnA⁷ has lethal phenotype

(Phillips et al., 2000)

Syt1^D27/Syt1^AD4, Syt1^elav.PD, stnA⁷ has uncoordinated phenotype

(Phillips et al., 2000)

Phenotype Manifest In

Enhanced by

Statement

Reference

Syt1^AD4/Syt1^N13 has embryonic/larval neuromuscular junction | larval stage phenotype, enhanceable by Syt7^M1/Syt7^M1

(Guan et al., 2020)

Suppressor of

Statement

Reference

(Tsai et al., 2019)

(Tsai et al., 2019)

(Tsai et al., 2019)

(Tsai et al., 2019)

(Tsai et al., 2019)

Syt1^AD4/Syt1^AD4 is a suppressor of synaptic vesicle | somatic clone | adult stage | progressive phenotype of Pect^omb593

(Tsai et al., 2019)

NOT Suppressor of

Statement

Reference

Syt1^AD4/Syt1^AD4 is a non-suppressor of synaptic vesicle | somatic clone | adult stage | progressive phenotype of Pect^omb593

(Tsai et al., 2019)

Additional Comments

Genetic Interactions

Statement

Reference

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

(Dickman et al., 2012)

Like Syt1^AD4/Syt1^N13 mutants alone, Syt1^AD4/Syt1^N13, Syt4^BA1 double mutants display robust asynchronous release. Paired-pulse facilitation remains intact in the double mutants, with enhanced facilitation as observed in Syt1^AD4/Syt1^N13 mutants alone. Also similar to Syt1^AD4/Syt1^N13 mutants alone, the release observed during paired-pulse stimulation in the double mutants remains asynchronous compared to wild type controls.

Syt1^AD4/Syt1^N13 mutants that also express Syt7^{dsRNA.Scer\UAS} under the control of Scer\GAL4^elav-C155 hatch and exhibit uncoordinated and slow movements (similar to Syt1^AD4/Syt1^N13 mutants alone), but then die during the first larval instar stage.

(Saraswati et al., 2007)

Overexpression of Syt7^Scer\UAS.cAa or SytIV^Scer\UAS.cLa, under the regulation of Scer\GAL4^elav-C155, in a syt^AD4/syt^N13 does not rescue any aspect of the behavioral phenotype. Overexpression of Syt7^Scer\UAS.cAa or SytIV^Scer\UAS.cLa, under the regulation of Scer\GAL4^elav-C155, in a syt^AD4/syt^N13 null mutant background has no effect on the synaptic transmission defects. Only slow release reflecting the asynchronous component of fusion is observed with the evoked EJP unchanged from the null mutant alone. Overexpression of SytIV^Scer\UAS.cLa, under the regulation of both Scer\GAL4^elav-C155 and Scer\GAL4^elav.PLu does not rescue the syt^AD4/syt^N13 phenotype. However, this overexpression does result in a 96% reduction in the expected Mendelian ratios.

(Adolfsen et al., 2004)

EJP amplitude at the neuromuscular junction is restored to near wild-type levels in syt^AD4 homozygous larvae if they are also expressing SytIV^Scer\UAS.cLa under the control of Scer\GAL4^elav.PLu. The increase in frequency of mEJPs is also rescued to wild-type in these larvae.

(Robinson et al., 2002)

The viability of syt^D27/syt^AD4 flies (rescued to adulthood by syt^elav.PD) is significantly reduced in combination with stnA⁶/Y or stnA⁷/Y. The few surviving males have an extreme behavioural phenotype and are very sedentary and severely uncoordinated (they are more uncoordinated than stnA⁺/Y ; syt^D27/syt^AD4 flies rescued to adulthood by syt^elav.PD). They die within 48 hours of eclosion. syt^D27/syt^AD4 females (rescued to adulthood by syt^elav.PD) and also heterozygous for stnA⁶ show abnormal behaviour, including a spread leg "spider-like" appearance and a slightly uncoordinated gait.

(Phillips et al., 2000)

Xenogenetic Interactions

Statement

Reference

Complementation and Rescue Data

Rescued by

Syt1^AD4/Syt1^N13 is rescued by Scer\GAL4^elav-C155/Syt1^UAS.Tag:MYC

(Montes-Chinea et al., 2018)

Syt1^AD4/Syt1^N13 is rescued by Scer\GAL4^elav-C155/Syt1^C2A-C2B.UAS

(Lee et al., 2013)

Syt1^AD4/Syt1^N13 is rescued by Scer\GAL4^elav-C155/Syt1^C2A*-C2B.UAS

(Lee et al., 2013)

Syt1^AD4 is rescued by Syt1^UAS.cSa/Scer\GAL4^elav.PLu

(Striegel et al., 2012)

Syt1^AD4 is rescued by Scer\GAL4^elav-C155/Syt1^UAS.cPa

(Paddock et al., 2011)

Syt1^AD4/Syt1^N13 is rescued by Syt1^UAS.cLa/Scer\GAL4^elav.PLu

(Yoshihara et al., 2010)

Syt1^AD4/Syt1^N13 is rescued by Syt1^UAS.cMa/Scer\GAL4^elav.PLu

(Poskanzer et al., 2006)

Syt1^AD4/Syt1^N13 is rescued by Scer\GAL4^elav-C155/Syt1^UAS.cLa

(Adolfsen et al., 2004)

Syt1^D27/Syt1^AD4 is rescued by Scer\GAL4^elav-C155/Syt1^{UAS.Tag:CALI(4C)}

(Marek and Davis, 2002)

Syt1^D27/Syt1^AD4 is rescued by Syt1^elav.PD

(Phillips et al., 2000)

Partially rescued by

Syt1^AD4 is partially rescued by Scer\GAL4^elav.PU/Syt1^UAS.cSb

(Shields et al., 2017)

Syt1^AD4/Syt1^N13 is partially rescued by Scer\GAL4^elav-C155/Syt1^C2A-C2B.UAS

(Lee et al., 2013)

Syt1^AD4/Syt1^N13 is partially rescued by Scer\GAL4^elav-C155/Syt1^{C2A*-C2B*.UAS}

(Lee et al., 2013)

Syt1^AD4/Syt1^N13 is partially rescued by Syt1^B-D3.4N.UAS/Scer\GAL4^elav.PLu

(Yoshihara et al., 2010)

Syt1^AD4/Syt1^N13 is partially rescued by Syt1^{C2A-D3.4N.UAS}/Scer\GAL4^elav.PLu

(Yoshihara et al., 2010)

Syt1^D27/Syt1^AD4 is partially rescued by Syt1^UAS.Tag:HA/Scer\GAL4^hs.PB

(Robinson et al., 2002)

Syt1^D27/Syt1^AD4 is partially rescued by Syt1^{D2N.UAS.Tag:HA}/Scer\GAL4^elav.PLu

(Robinson et al., 2002)

Syt1^D27/Syt1^AD4 is partially rescued by Syt1^{D2N.UAS.Tag:HA}/Scer\GAL4^hs.PB

(Robinson et al., 2002)

Syt1^AD4 is partially rescued by Syt1^UAS.cMa/Scer\GAL4^elav.PLu

(Mackler and Reist, 2001)

Syt1^AD4 is partially rescued by Syt1^KQ.UAS/Scer\GAL4^elav.PLu

(Mackler and Reist, 2001)

Syt1^AD4 is partially rescued by Syt1^elav.PD

(DiAntonio and Schwarz, 1994)

Not rescued by

Syt1^AD4/Syt1^N13 is not rescued by Scer\GAL4^elav-C155/Syt1^{I426K.UAS.Tag:MYC}

(Montes-Chinea et al., 2018)

Syt1^AD4 is not rescued by Scer\GAL4^elav.PU/Syt1^P-L.UAS

(Shields et al., 2017)

Syt1^AD4/Syt1^N13 is not rescued by Scer\GAL4^elav-C155/Syt1^C2A-C2B*.UAS

(Lee et al., 2013)

Syt1^AD4/Syt1^N13 is not rescued by Scer\GAL4^elav-C155/Syt1^{C2A*-C2B*.UAS}

(Lee et al., 2013)

Syt1^AD4/Syt1^N13 is not rescued by Scer\GAL4^elav-C155/Syt1^C2A.UAS

(Lee et al., 2013)

Syt1^AD4/Syt1^N13 is not rescued by Scer\GAL4^elav-C155/Syt1^C2A*.UAS

(Lee et al., 2013)

Syt1^AD4/Syt1^N13 is not rescued by Scer\GAL4^elav-C155/Syt1^C2B.UAS

(Lee et al., 2013)

Syt1^AD4/Syt1^N13 is not rescued by Scer\GAL4^elav-C155/Syt1^C2B*.UAS

(Lee et al., 2013)

Syt1^AD4/Syt1^N13 is not rescued by Scer\GAL4^elav-C155/Syt1^{C2A-C2A.UAS.Tag:HA}

(Lee et al., 2013)

Syt1^AD4/Syt1^N13 is not rescued by Syt1^{C2B-C2B.UAS.Tag:HA}/Scer\GAL4^elav-C155

(Lee et al., 2013)

Comments

The partial lethality of Syt1^AD4 homozygotes is partially rescued by Scer\GAL4^elav.PU-driven expression of Syt1^Scer\UAS.cSb but the lethality is not only rescued by Scer\GAL4^elav.PU-driven expression of Syt1^P-L.Scer\UAS but the lethality rate is further increased.

(Shields et al., 2017)

Scer\GAL4^elav-C155-mediated expression of Syt1^{C2A-C2B.Scer\UAS} restores synchronous neurotransmitter release (measured as eEJPs) at third instar NMJs in Syt1^N13/Syt1^AD4 animals. Partial rescue is seen at low (0.2mM) external Ca[2+], and near full rescue at high (1.0mM) external Ca[2+].

Scer\GAL4^elav-C155-mediated expression of Syt1^{C2A*-C2B.Scer\UAS} restores synchronous neurotransmitter release (measured as eEJPs) at third instar NMJs in Syt1^N13/Syt1^AD4 animals. Near full rescue is seen at both low (0.2mM) and high (1.0mM) external Ca[2+].

Scer\GAL4^elav-C155-mediated expression of Syt1^{C2A-C2B*.Scer\UAS} fails to restore synchronous neurotransmitter release (measured as eEJPs) at third instar NMJs in Syt1^N13/Syt1^AD4 animals at either low (0.2mM) or high (1.0mM) external Ca[2+].

Scer\GAL4^elav-C155-mediated expression of Syt1^{C2A*-C2B*.Scer\UAS} fails to restore synchronous neurotransmitter release (measured as eEJPs) at third instar NMJs in Syt1^N13/Syt1^AD4 animals at either low (0.2mM) or high (1.0mM) external Ca[2+].

Scer\GAL4^elav-C155-mediated expression of Syt1^C2A.Scer\UAS fails to restore synchronous neurotransmitter release (measured as eEJPs) at third instar NMJs in Syt1^N13/Syt1^AD4 animals at high (1.0mM) external Ca[2+].

Scer\GAL4^elav-C155-mediated expression of Syt1^{C2A*.Scer\UAS} fails to restore synchronous neurotransmitter release (measured as eEJPs) at third instar NMJs in Syt1^N13/Syt1^AD4 animals at high (1.0mM) external Ca[2+].

Scer\GAL4^elav-C155-mediated expression of Syt1^{C2A-C2A.Scer\UAS.T:Ivir\HA1} fails to restore synchronous neurotransmitter release (measured as eEJPs) at third instar NMJs in Syt1^N13/Syt1^AD4 animals at high (1.0mM) external Ca[2+].

Scer\GAL4^elav-C155-mediated expression of Syt1^C2B.Scer\UAS fails to restore synchronous neurotransmitter release (measured as eEJPs) at third instar NMJs in Syt1^N13/Syt1^AD4 animals at high (1.0mM) external Ca[2+].

Scer\GAL4^elav-C155-mediated expression of Syt1^{C2B*.Scer\UAS} fails to restore synchronous neurotransmitter release (measured as eEJPs) at third instar NMJs in Syt1^N13/Syt1^AD4 animals at high (1.0mM) external Ca[2+].

Scer\GAL4^elav-C155-mediated expression of Syt1^{C2B-C2B.Scer\UAS.T:Ivir\HA1} fails to restore synchronous neurotransmitter release (measured as eEJPs) at third instar NMJs in Syt1^N13/Syt1^AD4 animals at high (1.0mM) external Ca[2+].

Scer\GAL4^elav-C155-mediated expression of Syt1^{C2A-C2B.Scer\UAS} restores spontaneous neurotransmitter release frequency (measured as mEJPs) to control levels at third instar NMJs in Syt1^N13/Syt1^AD4 animals at low (0.2mM) external Ca[2+].

Scer\GAL4^elav-C155-mediated expression of Syt1^{C2A*-C2B.Scer\UAS} restores spontaneous neurotransmitter release frequency (measured as mEJPs) to control levels at third instar NMJs in Syt1^N13/Syt1^AD4 animals at low (0.2mM) external Ca[2+].

Scer\GAL4^elav-C155-mediated expression of Syt1^{C2A-C2B*.Scer\UAS} fails to restore spontaneous neurotransmitter release frequency (measured as mEJPs) to control levels at third instar NMJs in Syt1^N13/Syt1^AD4 animals at low (0.2mM) external Ca[2+].

Scer\GAL4^elav-C155-mediated expression of Syt1^{C2A*-C2B*.Scer\UAS} fails to restore spontaneous neurotransmitter release frequency (measured as mEJPs) to control levels at third instar NMJs in Syt1^N13/Syt1^AD4 animals at low (0.2mM) external Ca[2+]. Rather, mEJP frequency is dramatically increased.

Scer\GAL4^elav-C155-mediated expression of Syt1^{C2A-C2B.Scer\UAS} partially rescues the reduction in docked synaptic vesicles and vesicle density at type 1b boutons in Syt1^N13/Syt1^AD4 third instar larvae.

Scer\GAL4^elav-C155-mediated expression of Syt1^{C2A*-C2B*.Scer\UAS} partially rescues the reduction in docked synaptic vesicles and vesicle density at type 1b boutons in Syt1^N13/Syt1^AD4 third instar larvae.

Scer\GAL4^elav-C155-mediated expression of Syt1^C2A.Scer\UAS fails to restore spontaneous neurotransmitter release frequency (measured as mEJPs) to control levels at third instar NMJs in Syt1^N13/Syt1^AD4 animals at low (0.2mM) external Ca[2+].

Scer\GAL4^elav-C155-mediated expression of Syt1^{C2A*.Scer\UAS} fails to restore spontaneous neurotransmitter release frequency (measured as mEJPs) to control levels at third instar NMJs in Syt1^N13/Syt1^AD4 animals at low (0.2mM) external Ca[2+].

Scer\GAL4^elav-C155-mediated expression of Syt1^C2B.Scer\UAS fails to restore spontaneous neurotransmitter release frequency (measured as mEJPs) to control levels at third instar NMJs in Syt1^N13/Syt1^AD4 animals at low (0.2mM) external Ca[2+].

Scer\GAL4^elav-C155-mediated expression of Syt1^{C2B*.Scer\UAS} fails to restore spontaneous neurotransmitter release frequency (measured as mEJPs) to control levels at third instar NMJs in Syt1^N13/Syt1^AD4 animals at low (0.2mM) external Ca[2+].

Scer\GAL4^elav-C155-mediated expression of Syt1^{C2A-C2A.Scer\UAS.T:Ivir\HA1} fails to restore spontaneous neurotransmitter release frequency (measured as mEJPs) to control levels at third instar NMJs in Syt1^N13/Syt1^AD4 animals at low (0.2mM) external Ca[2+].

Scer\GAL4^elav-C155-mediated expression of Syt1^{C2B-C2B.Scer\UAS.T:Ivir\HA1} fails to restore spontaneous neurotransmitter release frequency (measured as mEJPs) to control levels at third instar NMJs in Syt1^N13/Syt1^AD4 animals at low (0.2mM) external Ca[2+].

Scer\GAL4^elav-C155-mediated expression of Syt1^{C2B-C2B.Scer\UAS.T:Ivir\HA1} fails to rescue the reduction in docked synaptic vesicles and vesicle density, or the increase in vesicle diameter, at type 1b boutons in Syt1^N13/Syt1^AD4 third instar larvae.

(Lee et al., 2013)

Expression of Syt1^Scer\UAS.cSa under the control of Scer\GAL4^elav.PLu in a Syt1^AD4 mutant background (i.e. where there is no endogenous Syt1) restores the synaptic synchronous evoked release to wild-type levels.

(Striegel et al., 2012)

Expression of Syt1^Scer\UAS.cLa under the control of Scer\GAL4^elav.PLu completely rescues the defects in the evoked synaptic currents recorded from muscle 6 of Syt1^N13/Syt1^AD4 embryos following motor nerve stimulation in 4mM extracellular Ca[2+]; evoked release is fully synchronous, and few asynchronous release events are seen in the rescued animals.

(Yoshihara et al., 2010)

Transgenic expression of syt^Scer\UAS.cLa (under the regulation of Scer\GAL4^elav-C155) in the null syt^AD4/syt^N13 background is able to partially restore all the behavioral defects observed. Overexpression of syt^Scer\UAS.cLa (under the regulation of Scer\GAL4^elav-C155) is able to restore evoked excitatory junctional potential (EJP) amplitudes to near wild-type levels in syt^AD4/syt^N13 mutants.

(Adolfsen et al., 2004)

Expression of syt^Scer\UAS.cMa under the control of Scer\GAL4^elav.PLu rescues the lethality of syt^AD4 flies; 85 +/- 6% of the expected number survive. The rescued adults are slightly uncoordinated. syt^AD4 homozygous larvae which are also expressing syt^Scer\UAS.cMa under the control of Scer\GAL4^elav.PLu have a mean excitatory junction potential (EJP) amplitude at the neuromuscular junction which is 67% of that of control larvae. The frequency of spontaneous miniature EJPs (mEJPs) in these larvae is slightly increased compared to controls (the difference is not statistically significant). The distribution of quantal sizes and the mean quantal size of the mEJPs is not different from controls. Expression of syt^KQ.Scer\UAS under the control of Scer\GAL4^elav.PLu partially rescues the lethality of syt^AD4 flies. The rescued animals are distinctly uncoordinated; syt^AD4 homozygous larvae which are also expressing syt^KQ.Scer\UAS under the control of Scer\GAL4^elav.PLu crawl sluggishly and move their mouth hooks at a slower frequency than normal. syt^AD4 homozygous adults which are also expressing syt^KQ.Scer\UAS under the control of Scer\GAL4^elav.PLu show slow, uncoordinated and arrhythmic limb placement when climbing. The mean excitatory junction potential (EJP) amplitude at the neuromuscular junction of syt^AD4 homozygous larvae which are also expressing syt^KQ.Scer\UAS under the control of Scer\GAL4^elav.PLu is significantly reduced compared to the mean EJP amplitude of syt^AD4 homozygous larvae which are also expressing syt^Scer\UAS.cMa under the control of Scer\GAL4^elav.PLu. The mean miniature EJP (mEJP) amplitude at the neuromuscular junction of syt^AD4 homozygous larvae which are also expressing syt^KQ.Scer\UAS under the control of Scer\GAL4^elav.PLu is not significantly different from the mean mEJP amplitude of syt^AD4 homozygous larvae which are also expressing syt^Scer\UAS.cMa under the control of Scer\GAL4^elav.PLu. The mean mEJP frequency at the neuromuscular junction of syt^AD4 homozygous larvae which are also expressing syt^KQ.Scer\UAS under the control of Scer\GAL4^elav.PLu is approximately twice that of syt^AD4 homozygous larvae which are also expressing syt^Scer\UAS.cMa under the control of Scer\GAL4^elav.PLu.

(Mackler and Reist, 2001)

Homozygous lethality can be rescued by syt^elav.PD. Rescued flies that emerge are lethargic and show an electrophysiological deficit due to insufficient syt. A second copy of syt^elav.PD improves viability and motor activity. ERGs of mutants carrying one copy of syt^elav.PD lack both on- and off-transients suggesting a disruption in synaptic communication. In mutants the evoked neurotransmitter release is decreased and spontaneous release in increased (intracellular recordings made from muscle 6).

(DiAntonio and Schwarz, 1994)

Images (0)

Mutant

Wild-type

Stocks (10)

Bloomington

606786

y¹ w^*; Syt1^AD4/CyO, y⁺

606805

y¹ w^*; Syt1^AD4 P{neoFRT}40A/CyO, y⁺

605933

y¹ w^*; Syt1^AD4/CyO, y⁺; P{UAS-syt.M}3

605932

y¹ w^*; Syt1^AD4 P{GAL4-elav.L}2/CyO, y⁺

605934

y¹ w^*; Syt1^AD4/CyO, y⁺; P{UAS-syt.KQ}59

606791

y¹ w^*; Syt1^AD4/CyO, y⁺; P{UAS-Syt1.D229E}2

606788

y¹ w^*; Syt1^AD4/CyO, y⁺; P{UAS-syt.B-D3,4N}87

606789

y¹ w^*; Syt1^AD4/CyO, y⁺; P{UAS-Syt1.A-R285Q}7

606790

y¹ w^*; Syt1^AD4/CyO, y⁺; P{UAS-Syt1.B-R419Q}3

606787

y¹ w^*; Syt1^AD4/CyO, y⁺; P{UAS-syt.B-D1,2N}104

Notes on Origin

Discoverer

Comments

Evoked synaptic transmission is suppressed but the frequency of individual miniature currents is increased 5-fold with respect to wild type, an increase in spontaneous vesicle release.

(Broadie et al., 1994)

Mutant phenotype can be rescued, when homozygous or in trans to syt^N6, by syt^elav.PD.

(Littleton et al., 1994)

External Crossreferences and Linkouts ( 0 )

Synonyms and Secondary IDs (9)

Reported As

Symbol Synonym

Syt 1^AD4

(Yoshihara et al., 2010)

Syt1^AD4

(Guan et al., 2020, Alicea et al., 2017, Guan et al., 2017, Poskanzer et al., 2006)

Syt1AD4

(Montes-Chinea et al., 2018)

Syt^AD4

(Ugur et al., 2017, Lohr et al., 2002)

synaptotagmin^AD4

(Tsai et al., 2019)

syt1^AD4

(Sauvola et al., 2021, Akbergenova et al., 2018, Lee and Littleton, 2015, Lee et al., 2013)

syt^AD4

(Bowers and Reist, 2020, Shields et al., 2020, Jin et al., 2018, Dickman et al., 2012, Haberman et al., 2012, Striegel et al., 2012, Mace et al., 2009, Mohrmann et al., 2008, Paddock et al., 2008, Saraswati et al., 2007, Dickman, 2006, Dickman et al., 2006, Hiesinger et al., 2006, Loewen et al., 2001)

syt^null

(Shields et al., 2017, Paddock et al., 2011, Mackler et al., 2002, Loewen et al., 2001, Mackler and Reist, 2001)

sytAD4

(Phillips et al., 2000)

Name Synonyms

Secondary FlyBase IDs

References (49)

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