COR27 and COR28 encode nighttime repressors integrating Arabidopsis circadian clock and cold response FA Summary It was noted that circadian components function in plant adaptation to diurnal temperature cycles and freezing tolerance. Our genome-wide transcriptome analysis revealed that evening-phased COR27 and COR28 mainly repress the transcription of clockassociated evening genes PRR5, ELF4 and cold-responsive genes. Chromatin immunoprecipitation indicated that CCA1 is recruited to the site containing EE elements of COR27 and COR28 promoters in a temperaturedependent way. Further genetic analysis shows COR28 is essential for the circadian function of PRR9 and PRR7. Together, our results support a role of COR27 and COR28 as nighttime repressors integrating circadian clock and plant cold stress responses.Functional clocks confer plants with fitness advantages in their stationary life, including enhanced photosynthesis and vegetative biomass, growth vigor in hybrids and allopolyploids, timely responses to pathogen, cold stress tolerance, photoperiodic flowering, and hormone signaling responses and other agronomic traits (Greenham and McClung 2015; Seo and Mas 2015). The Arabidopsis circadian clock, like the circadian clock found in many other model organisms, is composed of multiple interlocked transcriptional/translational feedback loops (TTFLs). Circadian-associated genes PSEU-DORESPONSE REGULATOR PRR9, PRR7, PRR5, CIRCADIAN CLOCK ASSOCIATED1 (CCA1), LATE ELONGATED HYPO-COTYL (LHY), LUX ARRHYTHMO (LUX), GIGANTEA (GI) and TIMING OF CAB EXPRESSION1 (TOC1, also called PRR1) play critical roles in plant cold responses (Hsu and Harmer 2014). Transcription of Cold-inducible C-repeat (CRT) /dehydration-responsive binding factors CBF1, CBF2, and CBF3 are upregulated in triple mutant prr9-11 prr7-10 prr5-10 (d975). Overexpression of CCA1a isoform results in higher levels of CBF1-3 and GI transcripts (Seo et al. 2012). Temperature-associated alternative splicing of CCA1, LHY, PRR9, PRR7, PRR5, PRR3, TOC1 mediate responses of circadian clock to diurnal temperature changes; especially CCA1b isoform modulates temperature signaling into clock and CCA1a isoform contributes to plant freezing tolerance (James et al. 2012; Seo et al. 2012). Recent study has established preliminary feedback of cold signaling to circadian clock; CBF1 can directly bind to the promoter of LUX, and coldacclimated lux mutants are sensitive to freezing stress (Chow et al. 2014). Despite the importance of the crosstalk between cold-responsive genes in planta, and that the control of low temperature-stress response is one of great interest for circadian research, a known comprehensive architecture of these interactions is still lacking (Bieniawska et al. 2008; Espinoza et al. 2010; Eriksson and Webb 2011; Keily et al. 2013).To identify new evening components contributing to the Arabidopsis circadian transcriptional network, we examined three online platforms of genome-wide expression profiles, NASCArrays (http://affymetrix. arabidopsis.info, closed),...
Brown and beige fat are specialized for energy expenditure by dissipating energy from glucose and fatty acid oxidation as heat. While glucose and fatty acid metabolism have been extensively studied in thermogenic adipose tissues, the involvement of amino acids in regulating adaptive thermogenesis remains little studied. Here, we report that asparagine supplementation in brown and beige adipocytes drastically upregulated the thermogenic transcriptional program and lipogenic gene expression, so that asparagine-fed mice showed better cold tolerance. In mice with diet-induced obesity, the asparagine-fed group was more responsive to b3-adrenergic receptor agonists, manifesting in blunted body weight gain and improved glucose tolerance. Metabolomics and 13 C-glucose flux analysis revealed that asparagine supplement spurred glycolysis to fuel thermogenesis and lipogenesis in adipocytes. Mechanistically, asparagine stimulated the mTORC1 pathway, which promoted expression of thermogenic genes and key enzymes in glycolysis. These findings show that asparagine bioavailability affects glycolytic and thermogenic activities in adipose tissues, providing a possible nutritional strategy for improving systemic energy homeostasis.
Brown and beige adipocytes harbor the thermogenic capacity to adapt to environmental thermal or nutritional changes. Histone methylation is an essential epigenetic modification involved in the modulation of nonshivering thermogenesis in adipocytes. Here, we describe a molecular network leading by KMT5c, a H4K20 methyltransferase, that regulates adipocyte thermogenesis and systemic energy expenditure. The expression of Kmt5c is dramatically induced by a β3-adrenergic signaling cascade in both brown and beige fat cells. Depleting Kmt5c in adipocytes in vivo leads to a decreased expression of thermogenic genes in both brown and subcutaneous (s.c.) fat tissues. These mice are prone to high-fat-diet-induced obesity and develop glucose intolerance. Enhanced transformation related protein 53 (Trp53) expression in Kmt5c knockout (KO) mice, that is due to the decreased repressive mark H4K20me3 on its proximal promoter, is responsible for the metabolic phenotypes. Together, these findings reveal the physiological role for KMT5c-mediated H4K20 methylation in the maintenance and activation of the thermogenic program in adipocytes.
Transcriptional feedback loops in Arabidopsis circadian clock is composed of more repressive components, while the knowledge of activation mechanism remains limited. We recently reported 2 members from a family of NIGHT LIGHT-INDUCIBLE AND CLOCK-REGULATED genes, LNK1 and LNK2, dynamically interact with morning-phased transcriptional factors, like CIRCADIAN CLOCK ASSOCIATED1 (CCA1), LATE ELONGATED HYPOCOTYL (LHY), REVEILLE8 (RVE8) and RVE4, and function as coactivators for the expression of TIMING OF CAB EXPRESSION1 (TOC1) and PSEUDO-RESPONSE REGULATOR5 (PRR5) via transcriptional factors RVE8 and RVE4. Here we provide evidence that both LNK1 and LNK2 play critical role in the transcriptional activation of PRR5, LNK1 may contribute more than LNK2 did under experimental conditions. We also identified that both LNK1 and LNK2 recruitment to the evening element of PRR5 promoter via LNK1-RVE8 or LNK2-RVE8 proteins complex through electrophoretic mobility shift assay. Therefore LNK1 and LNK2 function as coactivator of dawn-phased MYB-like transcription factors, such as RVE8 in morning complex to regulate the target genes expression.
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