The circadian system of plants regulates a wide range of rhythmic physiological and cellular output processes with a period of about 24 h. The rhythms are generated by an oscillator mechanism that, in Arabidopsis, consists of interlocking feedback loops of several components including CIRCADIAN CLOCK ASSOCIATED 1 (CCA1), LATE ELONGATED HYPOCOTYL (LHY), TIMING OF CAB EXPRESSION 1 (TOC1) and CCA1 HIKING EXPEDITION (CHE). Over recent years, researchers have gained a detailed picture of the clock mechanism at the resolution of the whole plant and several tissue types, but little information is known about the specificities of the clock mechanism at the level of individual cells. In this paper we have addressed the question of cell-type-specific differences in circadian systems. Using transgenic Arabidopsis plants with fluorescence-tagged CCA1 to measure rhythmicity in individual leaf cells in intact living plants, we showed that stomatal guard cells have a different period from surrounding epidermal and mesophyll leaf cells. By comparing transcript levels in guard cells with whole plants, we identified differences in the expression of some oscillator genes that may underlie cell-specific differences in clock properties. In addition, we demonstrated that the oscillators of individual cells in the leaf are robust, but become partially desynchronized in constant conditions. Taken together our results suggest that, at the level of individual cells, there are differences in the canonical oscillator mechanism that has been described for plants.
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http://dx.doi.org/10.1111/j.1365-313X.2011.04707.x | DOI Listing |
J Bras Pneumol
January 2025
. Departamento de Biologia Geral, Universidade Federal Fluminense, Niterói (RJ) Brasil.
Objective: Silicosis is a pneumoconiosis characterized by fibrosis of the lung parenchyma caused by the inhalation of silica particles. Silica dust inhalation is associated with inflammation and induction of oxidative stress in the lungs. This oxidative stress affects telomeres, which are short tandem DNA repeats that cap the end of linear chromosomes.
View Article and Find Full Text PDFSci Transl Med
January 2025
Department of Medicine, McMaster University, Hamilton, ON L8N 3Z5, Canada.
In prednisone-dependent severe asthma, uncontrolled sputum eosinophilia is associated with increased numbers of group 2 innate lymphoid cells (ILC2s). These cells represent a relatively steroid-insensitive source of interleukin-5 (IL-5) and IL-13 and are considered critical drivers of asthma pathology. The abundance of ILC subgroups in severe asthma with neutrophilic or mixed granulocytic (both eosinophilic and neutrophilic) airway inflammation, prone to recurrent infective exacerbations, remains unclear.
View Article and Find Full Text PDFSci Transl Med
January 2025
Hypothalamic Research Center, Department of Internal Medicine, UT Southwestern Medical Center, Dallas TX, 75390, USA.
Disruption of hypothalamic melanocortin 4 receptors (MC4Rs) causes obesity in mice and humans. Here, we investigated the transcriptional regulation of in the hypothalamus. In mice, we show that the homeodomain transcription factor Orthopedia (OTP) is enriched in MC4R neurons in the paraventricular nucleus (PVN) of the hypothalamus and directly regulates transcription.
View Article and Find Full Text PDFSci Robot
January 2025
Department of Bioengineering, Imperial College of London, London, UK.
Despite the advances in bionic reconstruction of missing limbs, the control of robotic limbs is still limited and, in most cases, not felt to be as natural by users. In this study, we introduce a control approach that combines robotic design based on postural synergies and neural decoding of synergistic behavior of spinal motoneurons. We developed a soft prosthetic hand with two degrees of actuation that realizes postures in a two-dimensional linear manifold generated by two postural synergies.
View Article and Find Full Text PDFElife
January 2025
Center for Spatial and Functional Genomics, The Children's Hospital of Philadelphia, Philadelphia, United States.
The prevalence of childhood obesity is increasing worldwide, along with the associated common comorbidities of type 2 diabetes and cardiovascular disease in later life. Motivated by evidence for a strong genetic component, our prior genome-wide association study (GWAS) efforts for childhood obesity revealed 19 independent signals for the trait; however, the mechanism of action of these loci remains to be elucidated. To molecularly characterize these childhood obesity loci, we sought to determine the underlying causal variants and the corresponding effector genes within diverse cellular contexts.
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