[2] Tobin’s lab was studying promoter fragments that contribute to light regulation of light-harvesting Chlorophyll A/B Binding Protein (LHCB), and noticed DNA-binding activity that had affinity for a specific light-responsive fragment of the LHCB promoter.
[7] The Arabidopsis central oscillator contains several proteins that reciprocally repress genes encoding each other to achieve a negative feedback loop necessary to generate circadian rhythms controlling many clock outputs.
Light induces its transcription, and mRNA levels peak at dawn along with Late Elongated Hypocotyl (LHY).
[11] Single loss of function mutants in both genes result in seemingly identical phenotypes.
Under constant light conditions, cca1 and lhy double loss of function mutants fail to maintain rhythms in clock controlled RNAs.
They show rhythms with a period of 1 day like their angiosperm homologs in 24-hour light-dark cycles or constant darkness.
[4] Mutants such as cca1-1 plants, which lack CCA1 protein, show short period phenotypes for the expression of several genes when assayed under constant light conditions.
They also have a period 3 hours shorter than that of the wild-type plant, which demonstrates that expression of LHY, its homolog, cannot fully compensate for the loss of the function of CCA1.
[13] Plants with non-functioning LHY and CCA1 show a wavy leaf phenotype in constant light conditions.
Mutants also have increased vascular pattern complexity in their leaves, with more areoles, branch points and free ends than wild-type Arabidopsis.