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Cargill, S. J.

Publications and source records attributed to Cargill, S. J..

2 recordsLinked to original sources

Crosstalk between salicylic acid signaling and the circadian clock promotes an effective immune response

The rotation of Earth creates a cycle of day and night, leading to predictable changes in environmental conditions. The circadian clock synchronizes an organism with these environmental changes and alters their physiology in anticipation. Prediction of the probable timing of pathogen infection enables plants to prime their immune system without wasting resources or sacrificing growth. Here, we explore the relationship between the immune hormone salicylic acid (SA), and the circadian clock in Arabidopsis. We found that SA altered circadian rhythmicity through the SA receptor and master transcriptional coactivator, NPR1. Reciprocally, the circadian clock gates SA-induced expression of NPR1-dependent immune genes. Furthermore, the clock gene CCA1 is essential for SA-induced immunity to the major bacterial plant pathogen Pseudomonas syringae. These results reveal new interactions between the circadian clock and SA signaling which produce an effective immune response. Understanding how and why the immune response in plants is linked to the circadian clock is crucial in working towards improved crop productivity.

plant biology↗

The methyl cycle is a conserved regulator of biological clocks.

The methyl cycle is a universally conserved metabolic pathway operating in prokaryotes and eukaryotes. In this pathway, the amino acid methionine is used to synthesize S-adenosylmethionine, the methyl donor co-substrate in the methylation of nucleic acids, histone and non-histone proteins and many other molecules within the cell. The methylation of nucleic acids and proteins is the foundation of epigenetic and epitranscriptomic regulations of gene expression, but whether the methyl cycle centrally regulates gene expression and function by controlling the availability of methyl moieties is poorly understood.\n\nFrom cyanobacteria to humans, a circadian clock that involves an exquisitely regulated transcription-translation-feedback loop driving oscillations in gene expression and orchestrating physiology and behavior has been described. We reported previously that inhibition of the methyl cycle in mammalian cells caused the lengthening of the period of these oscillations, suggesting the methyl cycle may indeed act as a central regulator of gene expression, at least in mammals. Here, we investigated whether the methyl cycle, given its universal presence among living beings, regulates the circadian clock in species across the phylogenetic tree of life.\n\nWe reveal a remarkable evolutionary conservation of the link between the methyl cycle and the circadian clock. Moreover, we show that the methyl cycle also regulates the somite segmentation clock, another transcription-translation negative feedback loop-based timing mechanism that orchestrate embryonic development in vertebrates, highlighting the methyl cycle as a master regulator of biological clocks.\n\nSIGNIFICANCE STATEMENTHere we reveal that the methyl cycle, a universal metabolic pathway leading to the synthesis of S-adenosylmethionine, the methyl donor co-substrate in virtually all transmethylation reactions within the cell, is a conserved regulator of biological clocks. These discoveries highlight the methyl cycle as a metabolic hub that regulates gene expression via the availability of methyl moieties for the methylation of nucleic acids, proteins and many other molecules with the cell.

evolutionary biology↗