Remarkably and consistent with the original hypothesis of Konopka that I per i SP I 01 i sp is a null mutant with no biological activity, this mutation creates a stop codon; there is therefore no wild-type PER encoded and perhaps no protein at all. This fear was not entirely unfounded as almost 25 years had passed between the publication of Konopka and Benzer on I period i and these Young lab publications on the second I Drosophila i clock gene I timeless i (I tim i). Keywords: circadian rhythm; Nobel lecture; period protein EN circadian rhythm Nobel lecture period protein 8732 8748 17 04/03/21 20210412 NES 210412 Circadian rhythms are present in most if not all animals, plants, and even photosynthetic cyanobacteria. The data in this paper also indicated that the I per i SP IS i sp protein is a hypomorph (has decreased function) rather than a hypermorph, with an increase in gene/protein activity as originally postulated by Konopka and Benzer.[11] The Young lab identified all 3 Konopka and Benzer mutations and also showed that more copies of I period i transgenes led to shorter periods.[29] At the risk of making a slight tangent to discuss much more recent data, we now have a quite sophisticated view of at least part of the PER molecular cycle, and these data underscore the hypomorphic or loss-of-function character of the I per i SP IS i sp protein. Because the TIM molecular weight was somewhat greater than that of PER and the two proteins associate in a yeast two hybrid assay,[42] TIM was an excellent candidate for the PER partner protein we had identified in fly head extracts.[Extracted from the article]

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