These genes are all paralogs of each other, and all repress the transcription of Circadian Clock Associated 1 (CCA1) and Late Elongated Hypocotyl (LHY) at various times throughout the day.
As a group, these genes are one part of the three-part repressilator system that governs the biological clock in plants.
Though their research that discovered PRR genes was primarily hailed during the early 2000s as informing the scientific community about the function of TOC1 (named APRR1 by the Mizuno lab), an additional pseudo-response regulator in the Arabidopsis thaliana biological clock,[3] the information about PRR genes that Matsushika and his team found deepened scientific understanding of circadian clocks in plants and led other researchers to hypothesize about the purpose of the PRR genes.
[1] Though current research has identified TOC1, PRR3, PRR5, PRR7, and PRR9 as of importance to the A. thaliana circadian clock mechanism, Matsushika et al. first categorized PRR genes into two subgroups (APRR1 and APRR2, the A stands for Arabidopsis) due to two differing amino acid structures.
[4] The negative feedback loops including PRR genes, proposed by Mizuno, were incorporated into a complex repressilator circuit by Andrew Millar’s lab in 2012.
PRR3, PRR5, PRR7 and PRR9 participate in the repressilator of a negative autoregulatory feedback loop that synchronizes to environmental inputs.
However, the inactivation of CCA1 and LHY in the PRR7/PRR9 loss-of-function mutants shows no change in period at high temperatures—this suggests that PRR7 and PRR9 are acting by overcompensation.
[9] The Constans (CO) is also indirectly regulated by the PRR proteins as well by setting up the molecular mechanism to dictate the photosensitive period in the afternoon.
[12] As PRR is a family of genes, several rounds mutant screening have been performed to identify each possible phenotype.
[14] The mechanistic details of each step in the plant biological clock repressilator system have yet to be fully understood.
[7] Additionally, identifying direct targets of PRR5, PRR7 and PRR9 that are not CCA1 and LHY will provide information about the molecular links from the PRRs to output genes like the flowering pathway and metabolism in mitochondria, which are CCA1-independent.