the displacement of the a-loop allows for the freeing of adjacent loops, further promoting the phosphorylation of kaic by kaia. evidence of this is shown through the demonstration that one kaia dimer is able to push kaic to a hyperphosphorylated state. kaia dimers exhibit a 95% association with kaic hexamers, in which more kaia dimers participate in interaction with kaic. the interaction between kaia and kaic is thus not a 1:1 interaction. kaia dimers likely flexibly associate and disassociate with kaic dimers rather than forming a stable complex, thus allowing for all the kaic subunits to be phosphorylated in the kai phosphorylation cycle. complexing model biochemical imaging revealed the assembly and disassembly of various kai complexes that form during circadian clock oscillations. during the process, kaia and kaib bind to sites on kaic; the model determines that kaic then becomes kaiac when kaia stimulates autophosphorylation, which then transforms into kaibc, kaiabc, and then returns to kaic as the cycle continues. hypothesized models “cyanobacteria are the simplest organisms known to exhibit circadian rhythms .” the transcription-translation based oscillator, in other words tto, is a proposed model that postulates kaic negatively regulates kaibc transcription and kaia positively regulates kaibc transcription. kai proteins don’t regulate circadian regulated genes, but do regulate genome wide gene expression in the cyanobacterial tto model. an example of this is the kaibc operon. it is still unclear how the transcription-translation feedback loop maintains periodicity and how it is flexible to environmental changes. since these proteins are essential for the organism to adapt to the environment, understanding the genes are imperative in circadian biology. in cyanobacterium synechococcus elongates (pcc 7942) kaia, kaib, and kaic are the necessary components that compose the circadian clock. the tto model of cyanobacteria is questionable due to the finding that phosphorylation of kaic oscillates regardless of transcription/translation of the kaibc operon. thus, it was postulated that the pacemaker is based upon kaic phosphorylation rather than transcription/translation feedback loop. kaia augments kaic autophosphorylation. kaia and atp promote the phosphorylation of t432. kaib mitigates the effect of kaia. thus, “autonomous oscillation of kaic phosphorylation could be generated by cooperation between kaia and kaib."