Model describing the
core circadian negative feedback loop of Neurospora. In the activation phase, CATP reduces the histone
occupancy on the frq promoter, which promotes WCC
binding and activation of frq transcription. After
transcription of frq mRNA, the nonoptimal codons
in frq mRNA regulate translation speed to allow proper
cotranslational folding of FRQ. The resulting FRQ protein is stabilized
by its interaction with FRH to form the FFC complex. In the repression
phase, FFC recruits casein kinases to phosphorylate PKA-primed WCs
and promotes degradation of frq mRNA by the exosome.
Phosphorylation of WCC inhibits its DNA binding activity and sequesters
it in the cytoplasm. FRQ is progressively phosphorylated by casein
kinases and degraded by the ubiquitin/proteasome system, a process
that is counterbalanced by the actions of PKA, PP1, and PP4. CSW-1
relocates nucleosomes to suppress frq activation,
whereas RCO-1 and CHD1 suppress WC-independent frq transcription to permit WCC-regulated frq transcription.
Dephosphorylation of WCC by PP2A and PP4 reactivates WCC to allow
reactivation of frq transcription.