A simplified version of the "green" plant clock, involving the master clock genes TOC1 and CCA1, has been revealed when the functional genomics and mathematical model approaches were combined.
Since the cryptochromes regulate the activity of BMAL1 and CLOCK, the proteins associated with the two master clock genes, these changes can have a significant effect on the circadian clock of an organism.
Furthermore, connections of SCN with other hypothalamic structures allow the master clock to synchronize other clock genes in the body [5, 6].
In conclusion, Li et al. [59] confirmed that during acute phase of sepsis in humans, there is an uncoupling of the central master clock and peripheral tissue-specific clock genes, associated with pro-inflammatory cytokine production.
Signals from the brain's master clock turn on and off 'core clock genes' in cells, which trigger cycles that cause some proteins to be produced in a circadian rhythm.
The master clock is regulated by four major groups of genes: Clock, Bmal1, Cry (Cryptochrome 1 and 2), and Per (Period 1 and 2).
Ten circadian clock genes have been identified in human peripheral tissues so far, including Period (Per-1-3), Crypto-chrome (Cry-1 and Cry-2), Clock, and Bmal1, which coordinate with the master clock located in the suprachiasmatic nuclei (SCN) of the anterior hypothalamus [3].
Izumo, Pejchal et al. used this approach to specifically disable the mouse's master clock and, unlike mice that completely lack the Bmal1 gene, mice with the brain-specific deletion were as healthy and lived as long as normal mice.
After the identification of the SCN master clock [ 5], the first component of the TTFL was identified as the gene Clock [ 6].
To further investigate the master clock, a typical approach has been made to disable it by deleting the genes for its components.
