Abstract
In Arabidopsis, the circadian rhythm is associated with multiple important biological processes and maintained by multiple interconnected loops that generate robust rhythms. The circadian clock central loop is a negative feedback loop composed of the core circadian clock components. TOC1 (TIMING OF CAB EXPRESSION 1) is highly expressed in the evening and negatively regulates the expression of CCA1 (CIRCADIAN CLOCK ASSOCIATED 1)/LHY (LATE ELONGATED HYPOCOTYL). CCA1/LHY also binds to the promoter of TOC1 and represses the TOC1 expression. Our recent research revealed that the histone modification complex comprising of LYSINE-SPECIFIC DEMETHYLASE 1 (LSD1)-LIKE 1/2 (LDL1/2) and HISTONE DEACETYLASE 6 (HDA6) can be recruited by CCA1/LHY to repress TOC1 expression. In this study, we found that HDA6, LDL1, and LDL2 can interact with TOC1, and the LDL1/2-HDA6 complex is associate with TOC1 to repress the CCA1/LHY expression. Furthermore, LDL1/2-HDA6 and TOC1 co-target a subset of genes involved in the circadian rhythm. Collectively, our results indicate that the LDL1/2-HDA6 histone modification complex is important for the regulation of the core circadian clock components.
Highlights
The circadian rhythm is an endogenous oscillation widely observed in plants, animals, fungi, and cyanobacteria (Edgar et al, 2012)
We demonstrated that LDL1/2-HISTONE DEACETYLASE 6 (HDA6) can interact with TOC1 to regulate the expression of CCA1 and LHY
We found that LDL1/2 and HDA6 interact with TOC1 to regulate the expression of CCA1 and LHY
Summary
The circadian rhythm is an endogenous oscillation widely observed in plants, animals, fungi, and cyanobacteria (Edgar et al, 2012). TOC1 is highly expressed in the evening, but low expressed at dawn (Alabadi et al, 2001). CCA1 and LHY are highly expressed in the morning, but low expressed at nightfall (Schaffer et al, 1998; Wang and Tobin, 1998; Alabadi et al, 2001). CCA1 and LHY bind to the evening element (EE) on the promoter of TOC1 to inhibit its expression (Schaffer et al, 1998; Wang and Tobin, 1998; Alabadi et al, 2001; Nagel et al, 2015). CCA1 and LHY were shown to repress the CHE expression by targeting the CHE promoter (Pruneda-Paz et al, 2009)
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