Sense-antisense transcription (driven by two convergent arrays of UAS sequence) of a 720 bp fragment of the 3' end of Shaw (starting at nucleotide 881 in exon 8 through to the end of the gene including approximately 110bp of 3' untranslated sequence) results in double stranded RNA (dsRNA) expression.
Flies expressing ShawdsRNA.Sym.Scer\UAS.cHa under the control of Scer\GAL4tim.PE exhibit short-period locomotor rhythms in constant dim white light, in contrast to control flies which largely show arrhythmic behavior in these conditions. These flies do not exhibit any difference in locomotor rhythms when kept in constant darkness, as compared to controls.
Flies expressing ShawdsRNA.Sym.Scer\UAS.cHa under the control of Scer\GAL4qsm-NP6258 exhibit locomotor rhythms in constant dim white light, in contrast to control flies which largely show arrhythmic behavior in these conditions.
The l-LNv neurons in flies expressing ShawdsRNA.Sym.Scer\UAS.cHa under the control of Scer\GAL4Pdf.PU exhibit depolarization of the nighttime (but not daytime) resting membrane potential, and an increased spontaneous firing rate during the night (but not during the day), as compared to wild type; these neurons also show a heightened response to blue light when tested during the daytime, as compared to wild type.
Expression of ShawdsRNA.Sym.Scer\UAS.cHa in all clock neurons (under the control of Scer\GAL4tim.PE) has no clear effect on locomotor rhythms in LD. The same is true when Scer\GAL80Pdf.PS is added to restrict expression.
Expression of ShawdsRNA.Sym.Scer\UAS.cHa in non-cry cells - a large fraction of the Dorsal Neurons, through Scer\GAL4tim.PE and Scer\GAL80cry.PS results in a lack of behavioural anticipation of the 'lights-on' transition in the morning, and only a marginal anticipation of the 'lights-off' transition in the evening. This abnormal behavioural pattern is most likely caused by a more central clock or clock-output defect, resulting in a drastically increased free-running period.
Reduction of Shaw expression in the DNs alone, through expression of ShawdsRNA.Sym.Scer\UAS.cHa (under the control of Scer\GAL4tim.PE and Scer\GAL80cry.PS) leads to a dramatic period lengthening of 3.5 to 4 hours.
Expression of ShawSym.Scer\UAS.cHa and Shawa.Sym.Scer\UAS.cHa in all clock neurons (under the control of Scer\GAL4tim.PE) has no clear effect on locomotor rhythms in LD. The same is true when Scer\GAL80Pdf.PS is added to restrict expression.
Expression of ShawSym.Scer\UAS.cHa and Shawa.Sym.Scer\UAS.cHa in non-cry cells - a large fraction of the Dorsal Neurons, through Scer\GAL4tim.PE and Scer\GAL80cry.PS results in a lack of behavioural anticipation of the 'lights-on' transition in the morning, and only a marginal anticipation of the 'lights-off' transition in the evening. This abnormal behavioural pattern is most likely caused by a more central clock or clock-output defect, resulting in a drastically increased free-running period.
Reduction of Shaw expression in the DNs alone, through expression of ShawSym.Scer\UAS.cHa and Shawa.Sym.Scer\UAS.cHa (under the control of Scer\GAL4tim.PE and Scer\GAL80cry.PS) leads to a dramatic period lengthening of 3.5 to 4 hours.
Associated with: Shawa.Sym.Scer\UAS.cHa.