The EE may be bound by Circadian Clock Associated 1 (CCA1) and Late Elongated Hypocotyl (LHY) proteins to suppress expression of LUX.
[7] The LUX ARRHYTHMO protein has a length of 323 amino acids and contains a Myb-like GARP family transcription factor DNA-binding domain.
[1][9] Although LUX and ELF4 are induced by low intensity, non-damaging UV-B radiation, the direct molecular mechanism of light input into the Arabidopsis circadian clock has yet to be elucidated.
[7] Experiments involving artificial microRNA (amiRNA) methods have shown that both NOX and LUX are required to recruit the EC to the PIF4 and PIF5 promoters.
RNAi experiments reducing NOX expression showed a continuation of circadian rhythms, whereas LUX null mutants are arrhythmic.
[1][7] Specific studies of LUX (and ELF3) orthologous mutant alleles have identified variants in flowering and photoperiod-dependent growth.
Like LUX, SN was found to be a major gene locus that controls regulation of circadian clock function and photoperiod-sensitive flowering.
[10] Gene loci orthologous to Arabidopsis ELF3, ELF4, and GI have also been found in P. sativum, named HIGH RESPONSE TO PHOTOPERIOD (HR), DIE NEUTRALIS (DNE), and LATE BLOOMER1 (LATE1) respectively.
The experiment leading to the discovery of HvLUX1 involved a mutation in the early maturity 10 (eam10) locus in the H. vulgare genome.
Via high throughput sequencing, HvLUX1 has been identified as a candidate gene for this locus, though its specific mechanism of action in the circadian clock has yet to be demonstrated.