A naturally occuring mutation of the core clock gene timeless in European Drosophila affects photoperiodic response

Surprise, surprise - a paper in Science is up there with a free online access (not the PDF, but the Full Text and that is something!):

A Molecular Basis for Natural Selection at the timeless Locus in Drosophila melanogaster:

Diapause is a protective response to unfavorable environments that results in a suspension of insect development and is most often associated with the onset of winter. The ls-tim mutation in the Drosophila melanogaster clock gene timeless has spread in Europe over the past 10,000 years, possibly because it enhances diapause. We show that the mutant allele attenuates the photosensitivity of the circadian clock and causes decreased dimerization of the mutant TIMELESS protein isoform to CRYPTOCHROME, the circadian photoreceptor. This interaction results in a more stable TIMELESS product. These findings reveal a molecular link between diapause and circadian photoreception.

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A reduced L-TIM/CRY interaction may explain the differences in the fly's circadian photoresponsiveness and the enhanced L-TIM stability. The observation that ls-tim females are more prone to diapause at any day length (1) is also consistent with the results presented here. As in the corresponding diapause profiles (1), the transformants conclusively reveal that the circadian photoresponsive phenotypes of natural tim variants are not due to linkage disequilibrium between tim and a nearby locus, but they are attributable to tim itself. Furthermore, the similarity in behavior of natural s-tim variants and P[S-TIM] transformants suggests that the residual putative truncated N-terminal 19-residue TIM product from the s-tim allele does not play any major role in the phenotypes we have studied (2).

It has been argued that the light sensitivity of the circadian clock needs to be abated in temperate zones because of the dramatic increase in summer day lengths in northern latitudes (18, 19). One mechanism for this process involves a reduced sensitivity to light-induced disturbance by having a higher pacemaker amplitude (18, 19). However, the amplitude of TIM cycling in DD was not significantly different between the two variants (fig. S1), nor were there any significant differences in amplitude or phase of the tim mRNA cycle between the s-tim and ls-tim genotypes (fig. S2). Another way to attenuate circadian photoresponsiveness in temperate zones may be by filtering light input into the clock. The molecular changes to the L-TIM protein may buffer the circadian response to light in ls-tim individuals, even in the presence of S-TIM, and may contribute to the positive Darwinian selection observed for ls-tim in the European seasonal environment (1).

So, here is another nice evidence for the connection between the core circadian clock and the photoperiodic response found in a nice evolutionary and ecological context.