A Database of Drosophila Genes & Genomes

FB2013_03, released May 7th, 2013
 

Allele Dmel\sei1

General Information
SymbolDmel\sei1SpeciesD. melanogaster
NameFlyBase IDFBal0015409
Feature typealleleAssociated geneDmel\sei
Also Known Asseits1
Map ( GBrowse ) GBrowse View Helpdetailed view FBal0015410 FBal0015409 FBal0015410
Allele class
Mutagenethyl methanesulfonate
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Description
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FB2013_03
FB2013_02
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Allele class
Mutagen
Mutations Mapped to the Genome
Type
Location
Additional Notes
References
point mutation
na_change=A19937797T
pr_change=K282|sei-PA,K282|sei-PB
reported_pr_change=K282@
Associated Sequence Data
DDBJ /
EMBL /
GenBank
DNA sequence
Protein sequence
Name
 
UniProtKB/Swiss-Prot
UniProtKB/TrEMBL
Progenitor genotype
Nature of the lesion
Statement
Reference
Amino acid replacement: K282. K282 lies before the first membrane-spanning segment.
Amino acid replacement: K282@. Resulting protein completely lacks the hydrophobic core that forms the transmembrane channel.
Cytology
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neuromuscular junction & synapse
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Statement
Reference
Intracellular recordings from mutant dorsal longitudinal muscles show bursts of spontaneous activity at 37[o]C.
sei[1]/sei[2] mutants display abundant small boutons, termed 'satellites', budding from the larger primary boutons along the branch axis. Such aberrant outgrowth is found at both type Ib and Is neuromuscular junctions in different muscles, e.g. 6/7 and 4. Upon closer examination, two distinct types of satellites are observed, one without a clear constriction between satellites and primary boutons, resembling yeast budding (type B satellites) and the other with a short but clear constriction or 'neck' (type M satellites). Type M satellites are more abundant than type B satellites in these mutants. There is also an overall increase in synaptic bouton number and terminal branching in these mutants. sei[1] mutants display significantly enhanced branching patterns along with a robust increase in mature bouton numbers, indicating that sei mutants do not fully prevent type M satellites from entering the successive growth steps. Exposure to high temperatures (29[o]C) for 2 hours during development fails to induce significant morphological changes in synaptic growth in sei[1] mutants. However, numbers of both B- and M-type satellites are drastically reduced after 5 hours of high temperature. Wild-type synapses do not exhibit this behaviour. Chronic high temperature treated (>5 hours) sei[1] mutants exhibit an unusual population of terminal branches consisting of thin strings of type M (and occasionally type B) satellites that are absent in controls. These unusual terminal branches contribute to the increased branching complexity in sei[1] mutants. These mutants also exhibit a decrease in primary bouton number.
sei[1] mutants display a 60% increase in bouton number at 31[o]C compared with 25[o]C.
sei1 flies do not show a significantly shortened lifespan. At day 37, these flies exhibit sporadic vacuoles throughout the central nervous system. Exposing these mutants to 40oC for 3 minutes results in seizures that last for up to a minute followed by paralysis. The severity of the phenotype progresses with age and daily exposure to the restrictive temperature.
sei1 mutants show behavioral convulsions after brief exposure to elevated temperature.
The courtship song parameters interpulse interval, cycles per pulse, interpulse frequency and amplitude of sound are normal in homozygous males at 25oC.
Substantial enhancement of spontaneous neural activity.
Heat induced expression of seihs.PW in adults is sufficient to restore normal locomotor function.
Homozygous larvae raised at the restrictive temperature (37oC for 6 hours/day from late embryogenesis through to third larval instar) show an increased frequency of ectopic neuromuscular synapses. Embryos raised at 18oC or 34oC show an increased frequency of immature filopodial contacts on muscle fibres 6 and 7 ("collateral sprouts") compared to wild-type embryos raised at the same temperature.
The delivery of an electrical buzz (50-400 msec) to the brain has no significant effect on sei1 mutant flies.
Spontaneous dorsal longitudinal muscle responses increase in frequency as the temperature is increased.
At temperatures >40oC, sei2 causes spontaneous activity in recordings from dorsal longitudinal flight muscles, to appear coincidentally with the heat-induced paralysis.
sei2 is semidominant in this respect and behavior of hyperploid adults exhibits dose dependence: sei2/sei2/+ flies become paralyzed, at 40oC, slightly less rapidly than homozygous mutants; sei2/+/+ paralyzed more slowly than sei2/+ but faster than wild-type.
Recordings of action potentials in the adult giant-fiber pathway reveal no decrement in sei2 at 40oC.
temperature-sensitive
 
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Statement
Reference
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Statement
Reference
sei1 has neuroanatomy defective | temperature conditional phenotype, suppressible by Syt4BA1
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Statement
Reference
hideNOT Enhancer of
Statement
Reference
sei1/sei[+] is a non-enhancer of short lived | dominant phenotype of AtpαDTS1
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Statement
Reference
sei1 is a suppressor of neuroanatomy defective phenotype of slo1
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Statement
Reference
sei1 has phenotype, enhanceable by e(sei)1
 
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Statement
Reference
sei1 has neuromuscular junction | temperature conditional phenotype, suppressible by Syt4BA1
sei1 has NMJ bouton | temperature conditional phenotype, suppressible by Syt4BA1
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Statement
Reference
hideSuppressor of
Statement
Reference
sei1 is a suppressor of neuromuscular junction phenotype of slo1
sei1 is a suppressor of NMJ bouton | supernumerary phenotype of slo1
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Statement
Reference
dao[b4] sei[1]/dao[g1] sei[1] double mutants show the same time to paralysis on shifting to the restrictive temperature as either single mutant.
When compared with single mutants, the combined mutational effects of sei[1]/slo[1] are not simply additive, with a further enhancement of some slo, but not sei phenotypes. Satellite abundance is less extreme in sei[1]/slo[1] double mutants compared to sei[1] mutants. There is a slight, but not significant, reduction in the numbers of both types B and M satellites. In contrast, the numbers of type M (but not type B) satellites and mature boutons are significantly greater in double mutants compared to slo single mutants.
sei[1] ; Syt4[BA1] double mutants exhibit no significant change in bouton number between 25[o]c and 31[o]C.
sei1/+; AtpαDTS1/+ double mutants have a similar lifespan to AtpαDTS1/+ single mutants.
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Statement
Reference
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Rescued by
Comments
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Discoverer
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Reduced level of saxitoxin binding in head membrane extracts and a decreased sodium current density in cultured embryonic neurons.
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hide Synonyms & Secondary IDs ( 4 )
Reported As
Symbol Synonym
sei1
 
Name Synonym
Secondary FlyBase IDs
hide References ( 19 )
Research paper
Guan et al., 2011, Learn. Mem. 18(4): 191--206
Altered gene regulation and synaptic morphology in Drosophila learning and memory mutants. [FBrf0213277]
Fergestad et al., 2010, Proc. Natl. Acad. Sci. U.S.A. 107(12): 5617--5621
A Drosophila behavioral mutant, down and out (dao), is defective in an essential regulator of Erg potassium channels. [FBrf0210402]
Lee and Wu, 2010, J. Neurosci. 30(47): 15821--15833
Orchestration of stepwise synaptic growth by k+ and Ca2+ channels in Drosophila. [FBrf0212405]
Barber et al., 2009, J. Cell Biol. 187(2): 295--310
Postsynaptic regulation of synaptic plasticity by synaptotagmin 4 requires both C2 domains. [FBrf0208997]
Fergestad et al., 2006, Genetics 172(2): 1031--1042
Neuropathology in Drosophila membrane excitability mutants. [FBrf0190718]
Ghezzi et al., 2004, Proc. Natl. Acad. Sci. U.S.A. 101(49): 17276--17281
slo K+ channel gene regulation mediates rapid drug tolerance. [FBrf0180655]
Hoeffer et al., 2003, J. Neurosci. 23(15): 6362--6372
Acute induction of conserved synaptic signaling pathways in Drosophila melanogaster. [FBrf0160607]
Peixoto and Hall, 1998, Genetics 148(2): 827--838
Analysis of temperature-sensitive mutants reveals new genes involved in the courtship song of Drosophila. [FBrf0101981]
Titus et al., 1997, J. Neurosci. 17(3): 875--881
The Drosophila erg K+ channel polypeptide is encoded by the seizure locus. [FBrf0092706]
Wang et al., 1997, J. Neurosci. 17(3): 882--890
The seizure locus encodes the Drosophila homolog of the HERG potassium channel. [FBrf0092719]
Jarecki and Keshishian, 1995, J. Neurosci. 15(12): 8177--8190
Role of neural activity during synaptogenesis in Drosophila. [FBrf0085285]
Pavlidis and Tanouye, 1995, J. Neurosci. 15(8): 5810--5819
Seizures and failures in the giant fiber pathway of Drosophila bang-sensitive paralytic mutants. [FBrf0083354]
Amichot et al., 1993, Insect Biochem. Mol. Biol. 23(3): 381--390
Transcription analysis of the para gene by in situ hybridisation and immunological characterization of ite expression product in wild-type and mutant strains of Drosophila. [FBrf0058672]
Elkins and Ganetzky, 1990, J. Neurogenet. 6: 207--219
Conduction in the giant nerve fiber pathway in temperature-sensitive paralytic mutants of Drosophila. [FBrf0052392]
O'Dowd and Aldrich, 1988, J. Neurosci. 8: 3633--3643
Voltage-clamp analysis of sodium channels in wild-type and mutant Drosophila neurons. [FBrf0048530]
Kasbekar et al., 1987, Genetics 116: 423--431
Enhancer of seizure: a new genetic locus in Drosophila melanogaster defined by interactions with temperature-sensitive paralytic mutations. [FBrf0046376]
Jackson et al., 1985, J. Neurosci. 5: 1144--1151
Genetic modifications of voltage-sensitive sodium channels in Drosophila: gene dosage studies of the seizure locus. [FBrf0043052]
Abstract
Wang et al., 1995, A. Dros. Res. Conf. 36: 108A
Genetic analysis and molecular cloning of the seizure gene. [FBrf0079594]
Nelson and Baird, 1985, Abstr. Soc. Neurosci. 11(1): 313
Action potentials persist at restrictive temperatures in temperature sensitive paralytic mutants of adult Drosophila. [FBrf0043557]