Nucleotide substitution: G?A. The mutation destroys the GT dinucleotide required for efficient splicing at the exon 2/intron 2 splice site.
Missense mutation destroying a splicing site.
G7770022A
G?A
G to A mutation in the GT splice donor sequence
Clkar homozygous adults flies either entrained to 12h:12h light:dark cycles and then moved to constant darkness or entrained to 12h:12h 24[o] C:29 [o]C temperature cycles and then moved to constant 24[o]C show arrhythmicity under both entrainment condition; temperature entrained individuals fail to show anticipatory activity to temperature transitions.
Homozygous flies are arrhythmic for locomotor activity.
Heterozygous animals exhibit a wild-type circadian locomotor rhythm. Homozygotes are arrhythmic. Clkar/Df(3L)HnD-1 and ClkJrk/Clkar animals are also arrhythmic. Under light:dark conditions homozygotes manifest a highly abnormal activity pattern: no lights-on startle response but a robust lights-off startle response. No measurable rhythmic activity is seen in constant darkness (DD), even during the first two days of DD.
Clkar has abnormal locomotor rhythm phenotype, suppressible by cycVP16.UAS/Scer\GAL4tim.PE
Expression of cycScer\UAS.T:Hsim\VP16 under the control of Scer\GAL4tim.PE fails to rescue circadian locomotor activity rhythms in Clkar flies under constant darkness conditions, but in light-dark conditions most of the abnormal features of locomotor activity seen in Clkar flies are rescued (higher diurnal rather than night activity as well as the lights-on startle response is restored).
Clkar is partially rescued by ClkΔ1-3.Tag:V5
Clkar is partially rescued by ClkΔ1-4.Tag:V5
Clkar is partially rescued by ClkUAS.Tag:HA/Scer\GAL4cry.PE
Clkar is not rescued by ClkUAS.Tag:HA/Scer\GAL4P2.4.Pdf
ClkT:SV5\V5 significantly rescues the arrhythmic locomotor behaviour of Clkar flies.
ClkΔ1-3.T:SV5\V5 poorly rescues the arrhythmic locomotor behaviour of Clkar flies.
ClkΔ1-4.T:SV5\V5 poorly rescues the arrhythmic locomotor behaviour of Clkar flies.