Rhythm defects caused by newly engineered null mutations in Drosophila's cryptochrome gene

Much of the knowledge about cryptochrome function in Drosophila stems from analyzing the cry(b) mutant. Several features of this variant's light responsiveness imply either that CRYb retains circadian-photoreceptive capacities or that additional CRY-independent light-input routes subserve these processes. Potentially to resolve these issues, we generated cry knock-out mutants (cry(0)' s) by gene replacement. They behaved in an anomalously rhythmic manner in constant light (LL). However, cry(0) flies frequently exhibited two separate circadian components in LL, not observed in most previous cry(b) analyses. Temperature-dependent circadian phenotypes exhibited by cry(0) flies suggest that CRY is involved in core pacemaking. Further locomotor experiments combined cry(0) with an externally blinding mutation (norpA(P24)), which caused the most severe decrements of circadian photoreception observed so far. cry(b) cultures were shown previously to exhibit either aperiodic or rhythmic eclosion in separate studies. We found cry(0) to eclose in a solidly periodic manner in light:dark cycles or constant darkness. Further-more, both cry(0) and cry(b) eclosed rhythmically in LL. These findings indicate that the novel cry(0) type causes more profound defects than does the cry(b) mutation, implying that CRYb retains residual activity. Because some norpA(P24) cry(0) individuals can resynchronize to novel photic regimes, an as-yet undetermined light-input route exists in Drosophila.