which LUX binds to the promoters of Phytochrome Interacting Factor 4 (PIF4) and Phytochrome Interacting Factor 5 (PIF5) and inhibits them. As a result, hypocotyl elongation is repressed in the early-evening. When the inhibition is alleviated late at night, the hypocotyl elongates. Photoperiod flowering is controlled by output gene Gigantea (GI). GI is activated at night and activates the expression of Constans (CO), which activates the expression of Flowering Locus T (FT). FT then causes flowering in long-days. Mammals Mammals evolved an endogenous timing mechanism to coordinate both physiology and behavior to the 24 hour period. In 2016, researchers identified a sequence of three subsequent inhibitions within this mechanism that they identified as a repressilator, which is now believed to serve as a major core element of this circadian network. The necessity of this system was established through a series of gene knockouts amongst cryptochrome (Cry), period (Per), and Rev-erb -- core mammalian clock genes whose knockouts lead to arrhythmicity. The model that these researchers generated includes Bmal1 as a driver of E-box mediated transcription, Per2 and Cry1 as early and late E-box repressors, respectively, as well as the D-box regulator Dbp and the nuclear receptor Rev-erb-α. The sequential inhibitions by Rev-erb, Per and Cry1 can generate sustained oscillations, and by clamping all other components except for this repressilator oscillations persisted with similar amplitudes and periods. All oscillating networks seem to involve any combination of these three core genes, as demonstrated in various schematics released by researchers. Recent Work The repressilator model has been used to model and study other biological pathways and systems. Since, extensive work into the repressilator’s modeling capacities has been performed. In 2003, the repressilator’s representation and validation of biological models, being a model with many variables, was performed using the Simpathica system, which verified that the model does indeed oscillate with all of its complexities. As stated in Elowitz and Leibler’s original work, the ultimate goal for repressilator research is to build an artificial circadian clock that mirrors its natural, endogenous counterpart. This would involve developing an artificial clock with reduced noise and temperature compensation in order to better understand circadian rhythms that can be found in every domain of life. Disruption of circadian rhythms may lead to loss of rhythmicity in metabolic and transcriptional processes, and even quicken the onset of certain neurodegenerative diseases such as Alzheimer's disease. In 2017, oscillators that generated circadian