Allele Dmel\bss¹

General Information
Symbol	Dmel\bss¹	Species	D. melanogaster
Name		FlyBase ID	FBal0001325
Feature type	allele	Associated gene	Dmel\bss

Allele class
Mutagen
Recent Updates
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FB2012_01
FB2011_10
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Nature of the Allele
Allele class
Mutagen
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
Cytology
Phenotypic Data
Phenotypic Class
	bang sensitive (Lee and Wu, 2002, Engel and Wu, 1994) bang sensitive \| semidominant (Pavlidis and Tanouye, 1995, Ganetzky and Wu, 1982, Hekmat-Scafe et al., 2005) behavior defective \| semidominant (Kulkarni et al., 1988) neurophysiology defective (Lee and Wu, 2002, Fergestad et al., 2006, Kuebler et al., 2001) neurophysiology defective \| semidominant (Pavlidis and Tanouye, 1995) paralytic (Lee and Wu, 2002, Hekmat-Scafe et al., 2010) paralytic \| semidominant (Pavlidis and Tanouye, 1995, Ganetzky and Wu, 1982)
Phenotype Manifest In
	abdominal 1 dorsal longitudinal muscle (Lee and Wu, 2002) central nervous system (Lee and Wu, 2002)
Detailed Description
	Statement Reference Rapid acute exposure to 100% CO[[2]], N[[2]] or He causes seizure-like activity in bss[1] mutants. Seizure-like activity is characterized by violent spinning of the flies accompanied by rapid uncoordinated movement of the wings, legs and abdomen. The initial bout of seizure-like activity, which usually occurs within 10 seconds of the onset of gas exposure, is followed by a period of paralysis in which the flies lay motionless. The paralysis is interrupted by bouts of delayed seizure-like activity that begins 30 to 60 seconds following the initial seizure-like activity. The delayed seizure-like activity is much more variable than the initial activity, as it often consists of multiple bouts of activity interspersed with periods of paralysis. Repeat exposure to CO[[2]] reduced the severity of seizure-like activity. bss[1] flies that are exposed to a second round of CO[[2]] exposure as soon as they recover from an initial acute exposure to CO[[2]], a process that takes approximately 3 minutes, are immobilized by the exposure but the amount of seizure-like activity is reduced. For example, following the first exposure, 76% of bss[1] flies display delayed seizure-like activity while following the second exposure only 61% of the flies display this activity. Five minutes after CO[[2]] induced seizure-like activity, only 6% of bss[1] flies are susceptible to mechanical shock. This resistance is transient as the vast majority of flies (>95%) are once again susceptible to mechanical shock 15 minutes following CO[[2]] exposure. Only 8% of bss[1] flies are susceptible to mechanical shock 3 minutes after N[[2]] induced seizure-like activity. Immediately following a mechanical shock, bss[1] flies display reduced susceptibility to CO[[2]] induced seizure-like activity. As soon as these flies recover from the initial mechanical shock (a process that takes approximately 4 minutes), only 65% of the flies exhibit delayed seizure-like activity in response to acute CO[[2]] exposure. Exposure of bss[1] flies to a 50/50 mix of CO[[2]] and O[[2]] results in initial and delayed seizure-like activity, indicating that hypercapnia is sufficient to trigger seizure-like activity in these flies as they have more than twice the level of atmospheric oxygen during exposure to the 50/50 mix. These flies are also susceptible to CO[[2]] induced anesthetization. Mixtures of 95% N[[2]] and 5% O[[2]] or 95% He and 5% O[[2]] do not trigger seizure-like activity in bss[1] flies. In fact, at 98% N[[2]] or He and 2% O[[2]], these flies do not exhibit seizure-like activity, although they do become sluggish. When the amount of O[[2]] is reduced even further to 1% or less, the flies begin to become anesthetized and in many cases exhibit seizure-like activity. Exposure of bss[1] to pure CO[[2]], He or O[[2]] for 2-5 minutes results in initial seizure-like activity but fails to generate the delayed seizure-like activity seen following acute exposure. After the initial seizure-like activity, the flies remain motionless throughout the duration of the 2- to 5-minute gas exposure. Once the gas exposure ends, the flies gradually recover normal function without displaying any delayed seizure-like activity. (Whelan et al., 2010) The giant fiber(GF)-dorsal longitudinal indirect flight muscle (DLM) neuronal circuit is more sensitive to seizure induction in mutants than in wild-type flies; seizures can be induced with high-frequency brain stimulation of shorter or less intensity in the mutant animals. The mutant animals show predominantly type II seizures. (Fergestad et al., 2006) More than 50% of bss¹/+ flies are bang sensitive. 100% of homozygous flies are bang sensitive. (Hekmat-Scafe et al., 2005) On mechanical agitation, bss¹ flies show a stereotypical behavioral sequence of initial spasm, paralysis, delayed spasm and recovery of normal posture. The two spasms are manifested by collapse of the body, high-frequency wing flapping, leg extension, and fully curved abdomen. Seizing females often lay eggs. Electroconvulsive stimulation delivered to the brain of bss¹ flies reproducibly induces the bang-sensitive repertoire of seizure behaviour; such electroconvulsive seizures can actually be induced in wild-type flies but this requires more extreme stimulus intensities than for bss¹ flies. The failure and recovery of the giant fibre (GF) pathway can be detected by recording the dorsal longitudinal muscle (DLM) physiological response. Following 1 Hz brain stimulation, bss¹ mutants have a significantly longer period of DLM response failure, and have an increased sensitivity for induction of this response failure, compared to wild type. Additionally, the maximal initial discharge induction is shifted toward lower stimulus intensities in the mutant flies. Delivery of a second stimulus after the onset of the delayed discharge (DD) phase of the DLM response causes a brief suppression of DD and a slight delay in response recovery, an effect that is more pronounced in bss¹ mutants than wild type. Delivery of a second stimulus after seizure recovery induces a refractory period during which DLM response failure is shortened and the DD stage is earlier and for a shorter duration; this refractory period is shorter in bss¹ flies than in wild type. Additionally, bss¹ flies show a rapid and abrupt restoration of full DD expression, compared to a more gradual DD restoration in wild-type. Electroconvulsive brain stimulation causes activity suppression and bursting events throughout the CNS; the period of activity suppression is longer in bss¹ mutants than wild-type flies. (Lee and Wu, 2002) The seizure threshold following short wavetrains of high-frequency electrical stimuli (0.5ms pulses at 200Hz for 300ms) is reduced in mutant flies (3.2 +/- 0.6 V) compared to controls. (Kuebler et al., 2001) Bang-sensitive mutant. Flies usually show abnormal spontaneous activity ("seizures") in the dorsal longitudinal muscle (DLM) lasting approximately 0.5-3 seconds after the delivery of an electrical buzz (50-400 msec) to the brain. Stimulation of the giant fibre (GF) usually fails to evoke DLM potentials following the buzz. This failure lasts for 112 +/- 70 seconds. There is a close correlation between the seizure and failure phenotypes; if a seizure occurs, a failure also occurs in greater than 95% of cases, while failures without seizures occurred in approximately 10% of cases. GF evoked responses by the DLM are abnormal during recovery from the buzz. After recovery, there is a refactory period during which a buzz is less effective at inducing seizures and failures. Failures are reduced in duration if the flies are also mutant for mle^nap-ts1. (Pavlidis and Tanouye, 1995) Physiological defect: a striking reduction of spike frequency in the anterior postalar (APA) and anterior notopleural (ANP) after mechanical stimulus. (Engel and Wu, 1994) Bang sensitive paralytic mutant. Paralysis lasts for 100-400 seconds, with the length of the paralysis increasing with age. There is a subsequent refractory period of several minutes before re-paralysis is effective. The larval neuromuscular junction preparation reveals abnormal long-term facilitation, and neuronal hyperexcitability. (Ganetzky and Wu, 1982)
External Data
Linkouts
Interactions
	Show the genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Enhanced by
Statement Reference bss¹ has bang sensitive phenotype, enhanceable by bas¹ (Lee and Wu, 2002) bss¹ has neurophysiology defective phenotype, enhanceable by bas¹ (Lee and Wu, 2002) bss¹ has paralytic phenotype, enhanceable by bas¹ (Lee and Wu, 2002)
NOT Enhanced by
Statement Reference bss¹ has behavior defective phenotype, non-enhanceable by Df(2L)TW1/+ (Fergestad et al., 2006)
Suppressed by
Statement Reference bss¹ has bang sensitive phenotype, suppressible \| partially by esg^EP633/Scer\GAL4^elav.PLu (Hekmat-Scafe et al., 2005) bss¹ has bang sensitive phenotype, suppressible \| partially by esg^EP2009/Scer\GAL4^elav.PLu (Hekmat-Scafe et al., 2005) bss¹ has bang sensitive phenotype, suppressible \| partially by esg^Scer\UAS.cFa/Scer\GAL4^elav.PLu (Hekmat-Scafe et al., 2005) bss¹ has bang sensitive phenotype, suppressible \| partially by Scer\GAL4^elav.PLu/sna^Scer\UAS.cFa (Hekmat-Scafe et al., 2005) bss¹ has bang sensitive phenotype, suppressible by esg^EP684/Scer\GAL4^elav.PLu (Hekmat-Scafe et al., 2005) bss¹ has neurophysiology defective phenotype, suppressible \| partially by shakB² (Kuebler et al., 2001) bss¹ has neurophysiology defective phenotype, suppressible by mle^nap-ts1 (Kuebler et al., 2001) bss¹ has paralytic phenotype, suppressible \| partially by kcc^Scer\UAS.cHb/Scer\GAL4^c739 (Hekmat-Scafe et al., 2010)
NOT suppressed by
Statement Reference bss¹ has bang sensitive phenotype, non-suppressible by Df(2L)osp29/+ (Hekmat-Scafe et al., 2005) bss¹ has bang sensitive phenotype, non-suppressible by esg^35Ce-1/esg[+] (Hekmat-Scafe et al., 2005) bss¹ has behavior defective phenotype, non-suppressible by Df(2L)TW1/+ (Fergestad et al., 2006)
Enhancer of
Statement Reference bss[+]/bss¹ is an enhancer of bang sensitive \| recessive phenotype of kcc^DHS1 (Hekmat-Scafe et al., 2006) bss¹ is an enhancer of bang sensitive phenotype of bas¹ (Lee and Wu, 2002) bss¹ is an enhancer of neurophysiology defective phenotype of bas¹ (Lee and Wu, 2002) bss¹ is an enhancer of paralytic phenotype of bas¹ (Lee and Wu, 2002)
Other
Statement Reference bss[+]/bss¹, kcc^DHS1 has bang sensitive \| dominant phenotype (Hekmat-Scafe et al., 2006) bss¹, mle^nap-ts1 has neurophysiology defective phenotype (Kuebler et al., 2001)
Phenotype Manifest In
Enhanced by
Statement Reference bss¹ has abdominal 1 dorsal longitudinal muscle phenotype, enhanceable by bas¹ (Lee and Wu, 2002)
Enhancer of
Statement Reference bss¹ is an enhancer of abdominal 1 dorsal longitudinal muscle phenotype of bas¹ (Lee and Wu, 2002)
Other
Statement Reference bas¹, bss¹ has mesothoracic extracoxal depressor muscle 66 phenotype (Lee and Wu, 2002, Lee and Wu, 2002) bss¹, mle^nap-ts1 has giant fiber neuron phenotype (Kuebler et al., 2001)
Additional Comments
Genetic Interactions
Statement Reference Expression of kcc[Scer\UAS.cHb] driven by Scer\GAL4[c739] significantly suppresses the bang-sensitive paralytic phenotype of bss[1] mutants. (Hekmat-Scafe et al., 2010) Df(2L)TW1/+ does not significantly alter the seizure phenotype of bss¹ hemizygotes. (Fergestad et al., 2006) Unlike either heterozygote alone, a bang sensitive phenotype is seen in kcc[DHS1]/+; bss[1]/+ adults (penetrance 48%). The penetrance of this phenotype rises to 77% in kcc[DHS1]/kcc[DHS1]; bss[1]/+ adults. (Hekmat-Scafe et al., 2006) The bang sensitivity of bss¹/+ flies (more than 50% of flies are bang sensitive) is substantially suppressed by the expression of one of esg^EP684, esg^EP2009 or esg^EP633 under the control of Scer\GAL4^elav.PLu. However, the 100% bang sensitivity of bss¹/bss¹ flies is not suppressed by the expression of one of esg^EP684, esg^EP2009 or esg^EP633 under the control of Scer\GAL4^elav.PLu. The bang sensitivity of bss¹/+ flies is partially suppressed by the expression of one of sna^Scer\UAS.cFa or esg^Scer\UAS.cFa under the control of Scer\GAL4^elav.PLu. The bang sensitivity of bss¹/+ flies is not significantly altered by esg^35Ce-1/+ or Df(2L)osp29/+. (Hekmat-Scafe et al., 2005) Following mechanical agitation, bss¹ bas¹ double mutant flies have a prolonged paralysis and take longer to recover following spasm than single mutants. These double mutants also have an enhanced susceptibility to electroconvulsion compared to single mutants with a prolonged DLM response failure. The sensitivity for response failure induction and maximal initial discharge induction is similar in the double mutants to bss¹ single mutants. Delivery of a second stimulus after the onset of DD causes a greater suppression of DD and a more delayed response recovery in double mutants than either single mutant. Additionally, delivery of a second stimulus after seizure recovery induces a shorter refractory period in bss¹ bas¹ double mutants. The jump muscle TTMs have an earlier response recovery following electroconvulsive stimuli, compared to DLMs; this effect is much more pronounced in bss¹ bas¹ mutants than in wild-type flies. Gynandromorph analysis shows that the recovery time of DLM responses to test stimuli applied to the brain is progressively lengthened as the number of bss¹ bas¹ mutant neurons in the GF pathway increases. (Lee and Wu, 2002) mle[nap-ts1] suppresses the reduced seizure threshold of bss[1] flies following high-frequency electrical stimuli, raising the seizure threshold to wild-type levels in the double mutant flies. shakB[2] does not suppress the reduced seizure threshold of bss[1] flies following high-frequency electrical stimuli. However, the double mutants do show a significant increase in the latency to seizure onset following 4V high-frequency stimuli compared to bss[1] single mutants. The double mutants show a reduction in spontaneous seizures during recovery from 4V high-frequency stimuli compared to bss[1] single mutants. The threshold for activation of the giant fiber in mutant animals following single stimulus pulses (0.2ms duration, 0.5Hz) is not significantly different from that of wild type. The threshold for activation of the giant fiber in bss[1] mle[nap-ts1] animals following single stimulus pulses (0.2ms duration, 0.5Hz) is elevated compared to wild type. (Kuebler et al., 2001)
Xenogenetic Interactions
Statement Reference
Complementation & Rescue Data
Comments
Stocks ( 0 )

Notes on Origin
Discoverer

Comments
	Complements: Dsp1¹. Dsp1¹ complements the bang sensitive paralysis of bss¹; the phenotype of bss¹/Dsp1¹ flies is the same as that of +/bss¹ flies. (Decoville et al., 2001) Phenotype suppressed by mle^nap-ts1, even at permissive temperatures. Double mutants do not pass out even when they are vibrated on the vortex mixer twice the usual amount of time. Double mutants have normal nerve activity and ejp. (Ganetzky and Wu, 1982)
External Crossreferences & Linkouts
Other Crossreferences

Linkouts

Synonyms & Secondary IDs ( 3 )
Reported As
Symbol Synonym	bas^MW1 (Hall, 1992) bss¹ (Fergestad et al., 2006, Hekmat-Scafe et al., 2006, Kuebler et al., 2001, Hekmat-Scafe et al., 2010, Whelan et al., 2010) bss^MW1 (Pavlidis and Tanouye, 1995, Engel and Wu, 1994, Kulkarni et al., 1988, Ganetzky and Wu, 1982)
Name Synonym
Secondary FlyBase IDs

References ( 13 )
Research paper	Hekmat-Scafe et al., 2010, Genetics 184(1): 171--183 Seizure sensitivity is ameliorated by targeted expression of k+-cl- cotransporter function in the mushroom body of the Drosophila brain. [FBrf0209683] Whelan et al., 2010, Brain Res. 1316C: 120--128 Sensitivity to seizure-like activity in Drosophila following acute hypoxia and hypercapnia. [FBrf0209944] Fergestad et al., 2006, Genetics 173(3): 1357--1364 Metabolic disruption in Drosophila bang-sensitive seizure mutants. [FBrf0194355] Hekmat-Scafe et al., 2006, J. Neurosci. 26(35): 8943--8954 Mutations in the K+/Cl- cotransporter gene kazachoc (kcc) increase seizure susceptibility in Drosophila. [FBrf0192588] Hekmat-Scafe et al., 2005, Genetics 169(3): 1477--1493 Seizure suppression by gain-of-function escargot mutations. [FBrf0183998] Lee and Wu, 2002, J. Neurosci. 22(24): 11065--11079 Electroconvulsive seizure behavior in Drosophila: analysis of the physiological repertoire underlying a stereotyped action pattern in bang-sensitive mutants. [FBrf0155894] Decoville et al., 2001, Genetics 157(1): 237--244 DSP1, an HMG-like protein, is involved in the regulation of homeotic genes. [FBrf0132331] Kuebler et al., 2001, J. Neurophysiol. 86(3): 1211--1225 Genetic suppression of seizure susceptibility in Drosophila. [FBrf0138446] 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] Engel and Wu, 1994, J. comp. Physiol. A. 175(3): 267--278 Altered mechanoreceptor response in Drosophila bang-sensitive mutants. [FBrf0076728] Kulkarni et al., 1988, Genetics 118: 267--285 The dissonance mutant of courtship song in Drosophila melanogaster: Isolation, behavior and cytogenetics. [FBrf0048204] Ganetzky and Wu, 1982, Genetics 100(4): 597--614 Indirect suppression involving behavioral mutants with altered nerve excitability in Drosophila melanogaster. [FBrf0038065]
Review	Hall, 1992, Lindsley, Zimm, 1992: 86 Entry for bss [FBrf0056777]

Allele Dmel\bss1

Allele Dmel\bss¹