Multiple labs identified the PRR genes as parts of the circadian clock in the 1990s. In 2000, Akinori Matsushika, Seiya Makino, Masaya Kojima, and Takeshi Mizuno were the first to understand PRR genes as pseudo-response repressor genes rather than as response regulator (ARR) genes. The factor that distinguishes PRR from ARR genes is the lack of a phospho-accepting aspartate site that characterizes ARR proteins. 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, 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. 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. The negative feedback loops including PRR genes, proposed by Mizuno, were incorporated into a complex repressilator circuit by Andrew Millar’s lab in 2012. The conception of the plant biological clock as made up of interacting negative feedback loops is unique in comparison to mammal and fungal circadian clocks which contain autoregulatory negative feedback loops with positive and negative elements (see "Transcriptional and non-transcriptional control on the Circadian clock page).