Allele Dmel\para^ts1

General Information
Symbol	Dmel\para^ts1	Species	D. melanogaster
Name		FlyBase ID	FBal0013491
Feature type	allele	Associated gene	Dmel\para
Also Known As	para^ts, para^ts-1

Allele class	heat sensitive hypomorphic allele - genetic evidence
Mutagen	ethyl methanesulfonate
Recent Updates
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FB2013_03
FB2013_02
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Nature of the Allele
Allele class	heat sensitive hypomorphic allele - genetic evidence (Ganetzky, 1984)
Mutagen	ethyl methanesulfonate (Suzuki et al., 1971, Pittendrigh 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	Dp(1;4)r⁺l (Falk and Halladay, 1986)
Nature of the lesion	Statement Reference Mutation within the intracellular S4-S5 linker, in domain I. (ffrench-Constant et al., 1998) Mutation is in the third intron. (Gamo et al., 1998)
Cytology
Phenotypic Data
Phenotypic Class
	behavior defective \| recessive \| heat sensitive (Hurd et al., 1996, Ganetzky, 1984) chemical resistant (Sharma and Kumar, 1999) chemical resistant \| recessive (Pittendrigh et al., 1997) chemical sensitive \| recessive (Leibovitch et al., 1995, Gamo et al., 1998) courtship behavior defective \| male \| recessive (Peixoto and Hall, 1998) lethal \| recessive \| heat sensitive (Lilly et al., 1994) neuroanatomy defective (Barber et al., 2009) neuroanatomy defective \| recessive \| heat sensitive (Jarecki and Keshishian, 1995) neuroanatomy defective \| third instar larval stage \| heat sensitive (Tsai et al., 2012) neurophysiology defective \| heat sensitive (Saitoe et al., 1997, Nitz et al., 2002, Sigrist et al., 2003, Ataman et al., 2008) neurophysiology defective \| recessive \| heat sensitive (Broadie and Bate, 1993) paralytic (Krishnan et al., 1996, Chandrashekaran and Sarla, 1993) paralytic \| adult stage \| recessive \| heat sensitive (Suzuki et al., 1971) paralytic \| heat sensitive (Dowse et al., 1995, Broadie and Bate, 1993, Fergestad et al., 2006, Hoeffer et al., 2003, Stimson et al., 2001, Falk et al., 1984, Rieckhof et al., 2003, Pavlidis and Tanouye, 1995, Elkins and Ganetzky, 1990, Sigrist et al., 2003, Budnik et al., 1990, Nelson and Wyman, 1990, Lagow et al., 2007, Wang et al., 2004) paralytic \| larval stage \| heat sensitive (Leiserson et al., 2011) paralytic \| recessive \| heat sensitive (Jarecki and Keshishian, 1995, Song and Tanouye, 2007) paralytic \| temperature conditional (Krishnan et al., 2001) viable (Saitoe et al., 1997, Broadie and Bate, 1993, Song and Tanouye, 2007) viable (with para^JS1) (Song and Tanouye, 2007)
Phenotype Manifest In
	adult brain (Fergestad et al., 2006) adult brain (with para^ts115) (Fergestad et al., 2006) adult heart \| P-stage (Johnson et al., 2002) neuromuscular junction (Broadie and Bate, 1993) neuromuscular junction \| temperature conditional (Barber et al., 2009) neuromuscular junction \| third instar larval stage \| heat sensitive (Tsai et al., 2012) synapse (Broadie and Bate, 1993)
Detailed Description
	Statement Reference When reared continuously at 22[o]C, neuromuscular junction size increases at a constant rate in mutant larvae, as occurs in wild type. However, when the are shifted to 29[o]C, NMJ size remains constant in the mutants, in contrast to the increase in size seen in wild type. (Tsai et al., 2012) para[ts1] mutants suppress temperature-induced synaptic outgrowth. (Barber et al., 2009) In controls, high K[+] stimulation results in the formation of "ghost boutons" - boutons containing synaptic vesicles but lacking active zones and presynaptic structures. But blocking action potentials in neurons by shifting para[ts1] larvae to restrictive temperatures prevents this. (Ataman et al., 2008) para[ts1]/Y males and para[ts1]/para[60] females are significantly more sensitive to isoflurane than control flies; the latency between nerve shock and excitatory junctional potential onset at the neuromuscular junction treated is significantly larger in the mutant flies than in controls following treatment with isoflurane. (Sandstrom, 2008) para[ts1] flies are completely paralysed at 38[o]C. (Lagow et al., 2007) para[ts1] homozygotes are viable but exhibit paralysis following heat shock. para[ts1]/para[JS1] flies are also viable but do not exhibit paralysis following heat shock. (Song and Tanouye, 2007) Neither para^ts1 nor para^ts1/para^ts115 flies show a significantly shortened lifespan. However, the brains of these flies show neurodegeneration. para^ts1 flies become instantly paralyzed upon exposure to a 3 minute 38^oC heat shock, but recover instantly when transferred to 22^oC. (Fergestad et al., 2006) para[ts1] flies are hypersensitive to isoflurane; isoflurane increases the delay from the stimulus to the onset of synaptic currents in both wild-type and mutant flies but the delay in response to isoflurane is increased in mutant axons compared to controls. (Sandstrom, 2005) sesB[1]/para[ts1] double mutants display no significant paralysis after heat shock (90s, 30[o]C) and vortexing (10s). Atpα[2206]/para[ts1] double mutants display no significant paralysis after heat shock (90s, 30[o]C) and vortexing (10s). (Trotta et al., 2004) para^ts1 mutants paralyse within seconds of exposure to 38^o. (Wang et al., 2004) para^ts1 mutant flies show flaccid paralysis when exposed to 30⁰C for 2 minutes. (Hoeffer et al., 2003) Mutant flies show a rapid onset of paralysis when placed at 38^oC. (Rieckhof et al., 2003) Like wild-type larvae, para^ts1 mutants exhibit an increase in quantal content and enhanced locomotor activity when moved from a food slurry environment at 18^oC to an agar plate at 22^oC. When the temperature is shifted to 34^oC for 20 minutes and maintained at 29^oC after this, para^ts1 larvae become paralysed, while wild-type larvae continue to show enhanced locomotion. After two hours of paralysis, quantal content levels of the para^ts1 mutants drop to those seen at 18^oC on the food slurry, while wild-type quantal content (following two hours of enhanced activity) is higher than at 22^oC. During the two hours at 29^oC, wild-type larvae show an increase in the number of large subsynaptic eIF-4E aggregates, while the amount of aggregates remain unchanged in the para^ts1 mutants. (Sigrist et al., 2003) Injection of 5-HT or norepinephrine increases the heart rate in para^ts1 mutant flies at 30^oC, and the change in rate is no different from that seen in wild-type controls. Injection of acetylcholine does no result in a significant change in heart rate in para^ts1 mutant flies at 30^oC (in contrast to wild-type controls which show an increase in heart rate when injected with acetylcholine). Injection of dopamine or octopamine increases the heart rate in para^ts1 mutant flies at 30^oC, but the increase is significantly less than that seen in wild-type controls. (Johnson et al., 2002) Spike-like potentials are seen when local field potential (LFP) recordings are made from the differential activity between one electrode place in between the mushroom bodies at approximately the level of the base of the calyces versus one placed in the lamina or medulla of the optic lobes. These spike-like potentials are significantly suppressed in para^ts1 in flies subjected to heat shock at 38^oC for 30 seconds, but are normal in flies kept at 25^oC. (Nitz et al., 2002) Life span at 28^oC is essentially the same as wild-type controls. (Palladino et al., 2002) Mutant flies are paralysed at 27^oC. (Krishnan et al., 2001) para^ts1 flies treated with sodium valproate (NaVP) do not show a reduction in body weight, in contrast to wild-type flies. Treatment of para^ts1 flies with NaVP causes an increase in mortality as is seen in wild-type flies. (Sharma and Kumar, 1999) The production of wing abnormalities induced by valproate in wild-type flies is suppressed by the para^ts1 mutation. (Sharma and Kumar, 1999) Flies are sensitive to ether (lower concentrations are required for anaesthesia compared to wild-type flies). (Gamo et al., 1998) Shows no temperature sensitive ERG on/off transients mutant phenotype. (Littleton et al., 1998) The difference in courtship song interpulse interval between para^ts1 and wild-type males shows a significant positive correlation with temperature, while the difference in courtship song amplitude between para^ts1 and wild-type males shows a significant negative correlation with temperature. (Peixoto and Hall, 1998) Homozygous flies show significant resistance to dichloro-diphenyl-trichloro ethane (DDT) compared to wild-type flies. (Pittendrigh et al., 1997) Temperature sensitive block or decrease is synaptic transmission at the neuromuscular junctions. Embryos shifted to restrictive temperature of 32^oC at 12hr AEL and kept at this temperature for the remainder of embryogenesis show no spontaneous movement nor were their tracheae inflated. Muscle pattern formation and shortening of the ventral nerve cord (VNC) is normal. Glutamate receptor clusters are found at the extrajunctional region, these are not seen in wild type embryos. Embryos reared at 30^oC show a few clusters at the extrajunctional region and some at the synaptic site. These embryos show low spontaneous movement and few hatch. At 25^oC receptors in the extrajunctional region disappear and are localised at te synaptic site. Embryos develop and hatch normally. 10hr heat shock at 34^oC after 12hr AEL causes receptor accumulation at the extrajunctional region. The number of receptor clusters increases at higher temperatures. Neural activity is required for receptor accumulation. (Saitoe et al., 1997) Temperature sensitive paralysis threshold is 32^oC. Flies become paralysed within 15 seconds of a temperature shift to 39^oC and recover completely within 15 seconds of shifting back to room temperature. (Hurd et al., 1996) Sub-anaesthetic concentration of carbon dioxide enhances the paralytic phenotype. (Krishnan et al., 1996) Mutation has no effect on larval heartbeat at temperatures between 20^oC and 37.5^oC. (Dowse et al., 1995) Homozygous larvae raised at the restrictive temperature (37^oC for 6 hours/day from late embryogenesis through to third larval instar) do not show an increased frequency of ectopic neuromuscular synapses, but do show an increased frequency of ectopic neuromuscular synapses if the larvae are also mutant for tipE^unspecified. Embryos raised at 34^oC show an increased frequency of immature filopodial contacts on muscle fibres 6 and 7 ("collateral sprouts") compared to wild-type embryos raised at 34^oC. (Jarecki and Keshishian, 1995) Homozygotes show increased sensitivity to halothane, chloroform and trichloroethylene in an inebriometer assay (an assay of geotactic and postural behaviour) compared to wild-type flies. Decapitated flies lose the halothane sensitive phenotype. (Leibovitch et al., 1995) The delivery of an electrical buzz (50-400 msec) to the brain has no significant effect on para^ts1 mutant flies. (Pavlidis and Tanouye, 1995) Lethal over para^sbl-3 and para^sbl-4. para^ts1 flies show a normal larval olfactory response to propionic acid at dilutions spanning three orders of magnitude. Transheterozygotes with para^sbl-1, para^sbl-2, para^sbl-5 and para^sbl-6 show normal olfactory response to 10^-1 propionic acid. Transheterozygotes of para^ts1 with para^sbl-1, para^sbl-5 and para^sbl-6 show a significant increase in temperature sensitive paralysis compared to para^ts1/+ controls. (Lilly et al., 1994) Adults are reversibly paralysed at 29^oC, at this temperature nerve conduction at the neuromuscular junction (NMJ) appears to be completely blocked. para^ts1/Df(1)D34 transheterozygotes die as first instar larvae. Homozygous embryos maintain periodic bursting activity with an excitatory junction current (EJC) amplitude similar to wild type, but bursting frequency and EJCs per burst are significantly reduced. Embryos hatch at 30^oC but show a dramatic reduction in hatching efficiency at 32^oC. Nerve conduction at the embryonic NMJ is reduced at 30^oC, nearly suppressed at 32^oC and blocked at 34^oC. Embryos reared at 34^oC for 8 hours from the onset of synaptogenesis exhibit distribution of glutamate receptors on the muscle, not localised at the NMJ. A shift in temperature mid-synaptogenesis does not affect receptor clustering at the NMJ. Synaptic morphology, at the light microscope level, of embryonic NMJs raised at the restrictive temperature is not significantly different from wild type. These hypoactive synapses occupy a smaller area of the muscle surface relative to wild type causing increased synaptic density (the branch and bouton numbers are not altered). (Broadie and Bate, 1993) para^ts1 mle^nap-ts1 double mutant bristle sensory cells in small-patch mosaic flies have normal branching and terminal arborisation patterns in the central nervous system. (Burg et al., 1993) Double mutants with mle^nap-ts1 or para^ts1 show no exaggeration of the paralytic phenotypes, nor any efect on their viability and fertility. These results suggest stmA does not interact with para or mle. (Chandrashekaran and Sarla, 1993) Flies become paralysed at 29^oC. (Budnik et al., 1990) Flies become paralysed at 29-31^oC. The long-latency response of the dorsal longitudinal muscle disappears abruptly as the temperature is increased to 31 +/- 1^oC, although the short-latency response is normal. (Elkins and Ganetzky, 1990) The temperature at which mutant flies become paralysed is dependent on the rearing temperature; flies raised at a low temperature (8^oC) become paralysed at a lower temperature than flies raised at a high (30^oC) temperature. Temperatures up to 7^oC above the paralytic temperature usually do not block the dorsal longitudinal muscle response to giant fibre stimulation. The jump muscle response is variable at this high temperature, some flies have a normal response, some have no response at all, and some have a reduced amplitude response. The interval from brain stimulation of the giant fibre to a response in the DLM or jump muscle is longer than in wild-type flies at all temperatures. Both the DLM and the jump muscle have a weaker following frequency than wild-type, which can be rescued by injecting 4-aminopyridine into mutant flies. (Nelson and Wyman, 1990) Reversible paralysis at 25^oC. (Falk et al., 1984) Lethal over In(1)D30, Df(1)r-D1, Df(1)D34 and Df(1)D7. (Ganetzky, 1984) Dissociated central nervous system cultures from para^ts1 larvae appear morphologically normal and cells have a similar survival rate to wild-type at both 22^oC and at the restrictive temperature of 35^oC. para^ts1 cell cultures show a significantly higher resistance to veratridine than wild-type cells at 22^oC, although the resistance is not as high as for mle^nap-ts1 cells. At 35^oC, the resistance of para^ts1 cells to veratridine increases to a level similar to mle^nap-ts1 cells. (Suzuki and Wu, 1984) Homozygous or hemizygous adults show normal walking and flying ability at 22^oC to 25^oC, but at higher temperatures become increasingly debilitated, and become completely paralysed in less than 5 seconds when shifted to 29^oC. This paralysis is reversible; mobility is recovered in less than 2 seconds when paralysed flies are shifted back to 22^oC. Paralysis and recovery can be induced repeatedly in the same individuals with no apparent harm. Although paralysis is initially complete at 29^oC, some recovery of movement is seen in flies kept at 29^oC, and after 30 minutes at 29^oC, flies can right themselves and have limited walking ability. Larval mobility is unaffected. (Suzuki et al., 1971) Marked reduction in number of embryonic neurons in cell culture expressing sodium currents in these alleles (O'Dowd et al., 1987; O'Dowd et al., 1989). temperature-sensitive
External Data
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Interactions
	Show the genetic interaction network for Enhancers & Suppressors
Phenotypic Class
NOT Enhanced by
Statement Reference para^ts1 has paralytic \| heat sensitive phenotype, non-enhanceable by stnB⁶/stnA⁶ (Stimson et al., 2001) para^ts1 has paralytic \| larval stage \| heat sensitive phenotype, non-enhanceable by Ncc69^r2 (Leiserson et al., 2011) para^ts1 has paralytic \| temperature conditional phenotype, non-enhanceable by awd^CM47 (Krishnan et al., 2001) para^ts1 has paralytic \| temperature conditional phenotype, non-enhanceable by awd^MSF15 (Krishnan et al., 2001) para^ts1 has paralytic \| temperature conditional phenotype, non-enhanceable by awd^MSM95 (Krishnan et al., 2001)
Suppressed by
Statement Reference para^ts1 has neuroanatomy defective \| temperature conditional phenotype, suppressible by Syt4^BA1 (Barber et al., 2009) para^ts1 has neuroanatomy defective \| third instar larval stage \| heat sensitive phenotype, suppressible by LanA^C01-190/Scer\GAL4^C57 (Tsai et al., 2012)
Enhancer of
Statement Reference para[+]/para^ts1 is an enhancer of paralytic \| heat sensitive phenotype of ST6Gal^S23 (Repnikova et al., 2010) para[+]/para^ts1 is an enhancer of short lived \| dominant phenotype of Atpα^DTS1 (Fergestad et al., 2006)
Suppressor of
Statement Reference para^ts1 is a suppressor of neurophysiology defective \| heat sensitive phenotype of Brkd^J29 (Montana and Littleton, 2004) para^ts1 is a suppressor of neurophysiology defective \| heat sensitive phenotype of Mhc⁵ (Montana and Littleton, 2004) para^ts1 is a suppressor of neurophysiology defective \| heat sensitive phenotype of Mhc^S1 (Montana and Littleton, 2004) para^ts1 is a suppressor of neurophysiology defective \| heat sensitive phenotype of Mhc^S2 (Montana and Littleton, 2004) para^ts1 is a suppressor of neurophysiology defective \| heat sensitive phenotype of Swg^X118 (Montana and Littleton, 2004) para^ts1 is a suppressor of paralytic \| conditional phenotype of Atpα²²⁰⁶ (Trotta et al., 2004) para^ts1 is a suppressor of paralytic \| conditional phenotype of sesB¹ (Trotta et al., 2004)
Other
Statement Reference Atpα^DTS2, para^ts1 has short lived phenotype (Fergestad et al., 2006, Fergestad et al., 2006) comt⁴, para^ts1 has paralytic \| heat sensitive phenotype (Littleton et al., 2001, Littleton et al., 2001) comt⁴, para^ts1 has paralytic phenotype (Littleton et al., 2001, Littleton et al., 2001) Khc⁶/Khc^BD, para^ts1 has lethal phenotype (Hurd et al., 1996, Hurd et al., 1996) mle^nap-ts1, para^ts1 has behavior defective \| dominant phenotype (Ganetzky, 1984) mle^nap-ts1, para^ts1 has lethal \| recessive phenotype (Ganetzky, 1984) mle^nap-ts1, para^ts1 has lethal phenotype (Ganetzky, 1984) mle^nap-ts1, para^ts1 has paralytic \| heat sensitive phenotype (Dowse et al., 1995)
Phenotype Manifest In
Enhanced by
Statement Reference para^ts1 has adult brain phenotype, enhanceable by Atpα^DTS1/Atpalpha[+] (Fergestad et al., 2006) para^ts1 has phenotype, enhanceable by Khc⁴ (Hurd et al., 1996) para^ts1 has phenotype, enhanceable by Khc⁵ (Hurd et al., 1996)
Suppressed by
Statement Reference para^ts1 has neuromuscular junction \| temperature conditional phenotype, suppressible by Syt4^BA1 (Barber et al., 2009) para^ts1 has neuromuscular junction \| third instar larval stage \| heat sensitive phenotype, suppressible by LanA^C01-190/Scer\GAL4^C57 (Tsai et al., 2012)
Enhancer of
Statement Reference para[+]/para^ts1 is an enhancer of adult brain phenotype of Atpα^DTS1 (Fergestad et al., 2006) para^ts1 is an enhancer of wing phenotype of Scer\GAL4^A307, Sh^{EKO.Scer\UAS.T:Avic\GFP-GL} (White et al., 2001)
Suppressor of
Statement Reference para^ts1 is a suppressor of indirect flight muscle \| heat sensitive phenotype of Brkd^J29 (Montana and Littleton, 2004) para^ts1 is a suppressor of indirect flight muscle \| heat sensitive phenotype of Mhc⁵ (Montana and Littleton, 2004) para^ts1 is a suppressor of indirect flight muscle \| heat sensitive phenotype of Mhc^S1 (Montana and Littleton, 2004) para^ts1 is a suppressor of indirect flight muscle \| heat sensitive phenotype of Mhc^S2 (Montana and Littleton, 2004) para^ts1 is a suppressor of indirect flight muscle \| heat sensitive phenotype of Swg^X118 (Montana and Littleton, 2004) para^ts1 is a suppressor of neuromuscular junction \| temperature conditional phenotype of Syt4^BA1 (Barber et al., 2009) para^ts1 is a suppressor of NMJ bouton \| temperature conditional phenotype of Syt4^BA1 (Barber et al., 2009)
Other
Statement Reference Ca-P60A^Kum170, comt⁶, para^ts1 has dorsal medial muscle \| heat sensitive phenotype (Hoeffer et al., 2003, Hoeffer et al., 2003) Ca-P60A^Kum170, comt⁶, para^ts1 has dorsal medial muscle phenotype (Hoeffer et al., 2003)
Additional Comments
Genetic Interactions
Statement Reference The reduction in neuromuscular junction size seen in para[ts1] larvae at 29[o]C is suppressed by expression of LanA[C01-190] under the control of Scer\GAL4[C57]. (Tsai et al., 2012) The severity of the temperature sensitive paralytic phenotype seen in ST6Gal[S23]/ST6Gal[S23] flies is enhanced by para[ts1]/+; the time for onset of paralysis at 38[o]C is reduced in the double mutant flies compared to the single mutant. (Repnikova et al., 2010) Synaptic outgrowth induced by expression of Syt4[wt.Scer\UAS] under the control of Scer\GAL4[Mhc.PW] is dramatically reduced in a para[ts1] background when animals are reared at 31[o]C compared with 25[o]C. (Barber et al., 2009) The short lived phenotype of Atpα^DTS1 heterozygotes is enhanced in para^ts1/+ flies. para^ts1; Atpα^DTS2 double mutants also have a short lifespan of <1 week. In addition to a shorter lifespan, para^ts1/+; Atpα^DTS1/+ double mutants show an increase in the severity of spongiform neuropathology of the brain at 16 days compared to brains from para^ts1/+ or Atpα^DTS1/+ single mutants. These double mutants show no significant change in temperature sensitivity compared to the single mutants. Like Atpα^DTS1 single mutants, para^ts1; Atpα^DTS1 mutants need several minutes to recover from a 3 minute 38^oC heat shock. (Fergestad et al., 2006) The characteristic contraction of Ca-P60A^unspecified larvae that is seen at the restrictive temperature for Ca-P60A^unspecified is abolished in Ca-P60A^unspecified ; para^ts1 double mutants if the double mutants are at a temperature that is restrictive for both Ca-P60A^unspecified and para^ts1, but is still seen if the double mutants are at a temperature that is restrictive for Ca-P60A^unspecified but permissive for para^ts1. (Sanyal et al., 2005) Suppression of Mhc⁵ seizure activity is observed in para^ts1 Mhc⁵/+ double mutant hemizygous males at 38^oC. (Montana and Littleton, 2004) comt⁶ para^ts1; Ca-P60A^Kum170 triple mutants do not show spontaneous DLM firing activity at 33⁰C like comt⁶ and Ca-P60A^Kum170 single mutants, but these triple mutants do show an increase of activity when shifted to 40⁰C, the restrictive temperature for para^ts1 mutants. (Hoeffer et al., 2003) comt⁴, para^ts1 double mutant animals exposed to 38^oC for 5 minutes show a rapid recovery from the paralysis phenotype when returned to the permissive temperature. After rapid recovery and normal behaviour, these flies suddenly re-paralyse several minutes later at the permissive temperature. (Littleton et al., 2001) 79% of para^ts1 flies expressing two copies of P{UAS-EKO⁺} (driven by Scer\GAL4^A307) fail to expand their wings. (White et al., 2001) Flies that are also Khc⁶/Khc^BD show synthetic lethality. (Hurd et al., 1996) Shows unconditional lethality when double mutant with mle^nap-ts1. Lethality is evident even when the flies are grown at 18^oC. Lethality acts before pupation, mostly in the larval stages. para^ts1 shows dominant effects on both behavior and viability in an mle^nap-ts1 background. (Ganetzky, 1984)
Xenogenetic Interactions
Statement Reference
Complementation & Rescue Data
Comments
Stocks ( 1 )
Kyoto	106393 para^ts1/C(1)DX, y¹ f¹
Notes on Origin
Discoverer

Comments
	Order of sensitivity to ether anaesthesia is (most sensitive to least sensitive): para^hd8 > para^ts3 > para^ts1. Order of sensitivity to heat induced paralysis is (lower temperature for 50% paralysis to higher temperature for 50% paralysis): para^ts3 > para^ts1 > para^hd8. (Gamo et al., 1998) At 32^oC postsynaptic GluRIIA expression is reduced and absent at 34^oC. (Broadie and Bate, 1993) dnc¹, para^ts1 and dnc¹, shi¹ double mutants show no more severe effect than either paralytic mutant alone. The para^ts1, stnA⁷ double mutant is no more inviable than stnA⁷ alone. (Sakai et al., 1989) Complements nonA⁹ in females heterozygous for both mutations. (Kulkarni et al., 1988) A haplo-specific lethal mutation. (Ganetzky, 1984) Does not suppress the Sh behavioural phenotype. (Ganetzky and Wu, 1982) Mosaic analysis shows that para⁺ head tissue is necessary for normal leg movement, and para⁺ thorax and leg tissue is required for the posture and normal movement of each leg. (Suzuki et al., 1971)
External Crossreferences & Linkouts
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Synonyms & Secondary IDs ( 6 )
Reported As
Symbol Synonym	para^TS1 (Rieckhof et al., 2003, Littleton et al., 2001, Littleton et al., 1998) para^ts-1 (Nelson and Wyman, 1990, Siddiqi and Benzer, 1976) para^ts1 (Hiesinger et al., 2006, Leiserson et al., 2011, Tsai et al., 2012, Lagow et al., 2007, Wang et al., 2004, Huang et al., 2006, Sandstrom, 2008, Sandstrom, 2005, Barber et al., 2009, Song and Tanouye, 2007, Popodi et al., 2010-, Trotta et al., 2004, Ataman et al., 2008, Fergestad et al., 2010, Repnikova et al., 2010) para^ts (Hoeffer et al., 2003, ffrench-Constant et al., 2004, Johnson et al., 2002, Dowse et al., 1995, Chandrashekaran and Sarla, 1993, Burg et al., 1993, Falk and Halladay, 1986, Falk et al., 1984, Ganetzky and Wu, 1982, Suzuki et al., 1971) parats1 (Ramazani and Atkinson, 2006)
Name Synonym	paralytic-ts (Richmond and Broadie, 2002)
Secondary FlyBase IDs

References ( 73 )

Generate a list of	All references relating to this allele ( 73 )

List References by type	Research paper ( 65 ) Review ( 2 ) Personal communication to FlyBase ( 1 ) Abstract ( 5 )
Recent research papers ( 2 )
	Tsai et al., 2012, Proc. Natl. Acad. Sci. U.S.A. 109(43): 17699--17704 Activity-dependent retrograde laminin A signaling regulates synapse growth at Drosophila neuromuscular junctions. [FBrf0219768] Leiserson et al., 2011, Glia 59(2): 320--332 Drosophila glia use a conserved cotransporter mechanism to regulate extracellular volume. [FBrf0212638] Show all research papers ...
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	All reviews listed in FlyBase were published before 2011 Show reviews ...

Allele Dmel\parats1

Allele Dmel\para^ts1