Allele Dmel\dysc^s168

General Information
Symbol	Dmel\dysc^s168	Species	D. melanogaster
Name		FlyBase ID	FBal0268517
Feature type	allele	Associated gene	Dmel\dysc

Allele class
Mutagen	Delta2-3
Recent Updates
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FB2013_03
FB2013_02
All updates	Click here to see a list of all updates to this record from FB2010_08 and on.
Nature of the Allele
Allele class
Mutagen	Delta2-3 (Jepson et al., 2012)
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 Insertion of P{XP} in an intron of dysc. dysc[s168] renders the long dysc isoforms undetectable, but expression of the short isoform is left intact. (Jepson et al., 2012)
Caused by insertion	P{XP}dysc^s168 (Jepson et al., 2012)
Cytology
Phenotypic Data
Phenotypic Class
	locomotor rhythm defective (with Df(3L)BSC614) (Jepson et al., 2012) locomotor rhythm defective (with dysc^c03838) (Jepson et al., 2012) locomotor rhythm defective (with dysc^c05107) (Jepson et al., 2012) locomotor rhythm defective \| recessive (Jepson et al., 2012) neurophysiology defective \| adult stage (Jepson et al., 2012)
Phenotype Manifest In

Detailed Description
	Statement Reference dysc[s168] homozygotes display arrhythmic locomotor patterns in constant dark conditions, with a minority showing weak rhythmicity. In contrast, the eclosion rhythm of these flies closely mirrors wild type controls. dysc[s168]/Df(3L)BSC614 animals display arrhythmic locomotor patterns in constant dark conditions. In contrast to wild type flies, dysc[s168] homozygotes do not exhibit anticipation of lights-on in 12 h light:dark conditions, while anticipation of lights-off is maintained. Overall daytime and nighttime activity is greater in these mutants compared to wild type in these conditions. dysc[s168]/dysc[c03838] and dysc[s168]/dysc[c05107] animals display arrhythmic locomotor patterns in constant dark conditions. Compared to wild type, dysc[s168] mutant Ilp2-positive neurons in adult brains show a much greater reduction in the outward current when the membrane potential is held at -30 mV, indicating a loss of non-activating currents. In contrast to wild type, the non-activating currents in dysc[s168] mutant Ilp2-positive neurons exhibit only a slight increase upon addition of CaCl[[2]]. Whereas application of 1 mM tetrathylammonium (a blocker of slo channels) reduces the total outward current by 63% in wild type neurons, it produces only a 17% reduction in dysc[s168] neurons. (Jepson et al., 2012)
External Data
Linkouts
Interactions
Phenotypic Class
Phenotype Manifest In
Additional Comments
Genetic Interactions
Statement Reference
Xenogenetic Interactions
Statement Reference
Complementation & Rescue Data
Rescued by	dysc^s168/dysc^c03838 is rescued by dysc^Scer\UAS.g/Scer\GAL4^C164 (Jepson et al., 2012) dysc^s168/dysc^c03838 is rescued by dysc^Scer\UAS.g/Scer\GAL4^dysc.PJ (Jepson et al., 2012) dysc^s168/dysc^c03838 is rescued by dysc^Scer\UAS.g/Scer\GAL4^elav.PU (Jepson et al., 2012)
Not rescued by	dysc^s168/dysc^c03838 is not rescued by dysc^Scer\UAS.g/Scer\GAL4^c061 (Jepson et al., 2012) dysc^s168/dysc^c03838 is not rescued by dysc^Scer\UAS.g/Scer\GAL4^c107 (Jepson et al., 2012) dysc^s168/dysc^c03838 is not rescued by dysc^Scer\UAS.g/Scer\GAL4^c819 (Jepson et al., 2012) dysc^s168/dysc^c03838 is not rescued by dysc^Scer\UAS.g/Scer\GAL4^dimm-929 (Jepson et al., 2012) dysc^s168/dysc^c03838 is not rescued by dysc^Scer\UAS.g/Scer\GAL4^ey-OK107 (Jepson et al., 2012) dysc^s168/dysc^c03838 is not rescued by dysc^Scer\UAS.g/Scer\GAL4^how-24B/Scer\GAL4^how-24B (Jepson et al., 2012) dysc^s168/dysc^c03838 is not rescued by dysc^Scer\UAS.g/Scer\GAL4^Ilp2.PR (Jepson et al., 2012) dysc^s168/dysc^c03838 is not rescued by dysc^Scer\UAS.g/Scer\GAL4^P2.4.Pdf (Jepson et al., 2012) dysc^s168/dysc^c03838 is not rescued by dysc^Scer\UAS.g/Scer\GAL4^repo.PU (Jepson et al., 2012) dysc^s168/dysc^c03838 is not rescued by dysc^Scer\UAS.g/Scer\GAL4^Tab2-201Y (Jepson et al., 2012) dysc^s168/dysc^c03838 is not rescued by dysc^Scer\UAS.g/Scer\GAL4^tim.PE (Jepson et al., 2012) dysc^s168/dysc^c03838 is not rescued by dysc^Scer\UAS.g/Scer\GAL4^VGlut-OK371 (Jepson et al., 2012) dysc^s168/dysc^c03838 is not rescued by Scer\GAL4^elav.PU/dysc^Scer\UAS.f (Jepson et al., 2012)
Comments	Scer\GAL4[elav.PU]-, Scer\GAL4[dysc.PJ]-, or Scer\GAL4[C164]-mediated expression of dysc[Scer\UAS.g] rescues the locomotor rhythm defects of dysc[c03838]/dysc[s168] animals. Scer\GAL4[elav.PU]-mediated expression of dysc[Scer\UAS.f] does not rescue the locomotor rhythm defects of dysc[c03838]/dysc[s168] animals. (Jepson et al., 2012)
Stocks ( 0 )

Notes on Origin
Discoverer

Comments
	Precise excision of the P{XP} element (as in dysc[pr9e]) reverts the locomotor rhythm phenotype. (Jepson et al., 2012)
External Crossreferences & Linkouts
Other Crossreferences

Linkouts

Synonyms & Secondary IDs ( 2 )
Reported As
Symbol Synonym	dysc^s168 (Jepson et al., 2012)
Name Synonym	dyschronic^s168 (Jepson et al., 2012)
Secondary FlyBase IDs

References ( 1 )
Research paper	Jepson et al., 2012, PLoS Genet. 8(4): e1002671 dyschronic, a Drosophila Homolog of a Deaf-Blindness Gene, Regulates Circadian Output and Slowpoke Channels. [FBrf0218124]

Allele Dmel\dyscs168

Allele Dmel\dysc^s168