Reversible post-transcriptional modifications on messenger RNA emerge as prevalent phenomena in RNA metabolism. The most abundant among them is N6-methyladenosine (m6A) which is pivotal for RNA metabolism and function; its role in stress response remains elusive. We have discovered that in response to oxidative stress, transcripts are additionally m6A modified in their 5' vicinity. Distinct from that of the translationally active mRNAs, this methylation pattern provides a selective mechanism for triaging mRNAs from the translatable pool to stress-induced stress granules. These stress-induced newly methylated sites are selectively recognized by the YTH domain family 3 (YTHDF3) "reader" protein, thereby revealing a new role for YTHDF3 in shaping the selectivity of stress response. Our findings describe a previously unappreciated function for RNA m6A modification in oxidative-stress response and expand the breadth of physiological roles of m6A.

Biotin affects gene expression at both the transcriptional and the posttranscriptional level; biotin metabolites might have biotin-like activities with regard to gene expression. Here, human hepatocarcinoma (HepG2) cells were used (i) to identify clusters of biotin-dependent genes, (ii) to determine whether the naturally occurring metabolite bisnorbiotin affects gene expression and (iii) to determine whether biotin and bisnorbiotin affect the expression of genes coding for ribosomal subunits and translation initiation factors. HepG2 cells were cultured in media containing deficient (0.025 nmol/L), physiological (0.25 nmol/L, control) and pharmacological (10 nmol/L) concentrations of biotin; a fourth treatment group consisted of cells cultured in biotin-deficient medium (0.025 nmol/L) supplemented with bisnorbiotin (0.225 nmol/L). Gene expression was quantified by using DNA microarrays and reverse transcriptase polymerase chain reaction. The expression of 1803 genes depended on biotin concentrations in culture media; the expression of 618 genes depended on bisnorbiotin. Biotin deficiency was associated with increased expression of a gene cluster encoding ribosomal subunits and eukaryotic translation initiation factor 5A; this effect was reversed by supplementation with biotin and bisnorbiotin. Additional prominent clusters of (bisnor)biotin-dependent genes included DNA-, RNA-, and nucleotide-binding proteins, consistent with a role for biotin in cell signaling and gene expression. Collectively, these data suggest that bisnorbiotin has biotin-like activities regarding gene expression, and that clusters of (bisnor)biotin-dependent genes include genes that play roles in translational activity.

Diet is a key lifestyle component that influences metabolic health through several factors, including total energy intake and macronutrient composition. While the impact of caloric intake on gene expression and physiological phenomena in various tissues is well described, the influence of dietary macronutrient composition on these parameters is less well studied. Here, we use the Nutritional Geometry framework to investigate the role of macronutrient composition on metabolic function and gene regulation in adipose tissue. Using ten isocaloric diets that vary systematically in their proportion of energy from fat, protein, and carbohydrates, we find that gene expression and splicing are highly responsive to macronutrient composition, with distinct sets of genes regulated by different macronutrient interactions. Specifically, the expression of many genes associated with Bardet-Biedl syndrome is responsive to dietary fat content. Splicing and expression changes occur in largely separate gene sets, highlighting distinct mechanisms by which dietary composition influences the transcriptome and emphasizing the importance of considering splicing changes to more fully capture the gene regulation response to environmental changes such as diet. Our study provides insight into the gene regulation plasticity of adipose tissue in response to macronutrient composition, beyond the already well-characterized response to caloric intake.

Parent-of-origin effects are unexpectedly common in complex traits, including metabolic and neurological traits. Parent-of-origin effects can be modified by the environment, but the architecture of these gene-by-environmental effects on phenotypes remains to be unraveled. Previously, quantitative trait loci (QTL) showing context-specific parent-of-origin effects on metabolic traits were mapped in the F16 generation of an advanced intercross between LG/J and SM/J inbred mice. However, these QTL were not enriched for known imprinted genes, suggesting another mechanism is needed to explain these parent-of-origin effects phenomena. We propose that non-imprinted genes can generate complex parent-of-origin effects on metabolic traits through interactions with imprinted genes. Here, we employ data from mouse populations at different levels of intercrossing (F0, F1, F2, F16) of the LG/J and SM/J inbred mouse lines to test this hypothesis. Using multiple populations and incorporating genetic, genomic, and physiological data, we leverage orthogonal evidence to identify networks of genes through which parent-of-origin effects propagate. We identify a network comprised of three imprinted and six non-imprinted genes that show parent-of-origin effects. This epistatic network forms a nutritional responsive pathway and the genes comprising it jointly serve cellular functions associated with growth. We focus on two genes, Nnat and F2r, whose interaction associates with serum glucose levels across generations in high-fat-fed females. Single-cell RNAseq reveals that Nnat expression increases and F2r expression decreases in pre-adipocytes along an adipogenic trajectory, a result that is consistent with our observations in bulk white adipose tissue.

Food is a physiological necessity for humans and is built on and permeated by many different biological, economic, social, and cultural symbols and phenomena. The basic conditions for adequate nutrition should be associated with cultural and financial values, physical accessibility, flavor, variety, color, and harmony and based on consumption of foods, not exclusively on nutrients. However, changes to the population's profile of consumption and dietary habits are founded on the process of urbanization and industrialization, which plays a fundamental role in this phenomenon, causing lifestyle changes that are linked with stimulus of consumption of industrialized products, with publicity, and with mass marketing. The objective of the study was to investigate the profile of the dietary habits of workers from different occupational categories in Brazil, with a sample of 13 articles. Moreover, research shows that many different categories of workers are subject to nutritional losses because of this new lifestyle. Searches were run on the Google Scholar, LILACS, and SciELO databases for publications during the last 5 years, identifying more than 15 thousand articles, 13 of which were selected as fitting the criteria chosen. Data were collected in April and May of 2020. The inclusion criteria were articles published in Portuguese with the full text available. Exclusion criteria were duplicates and studies with seniors and/or children. It was concluded that the dietary habits of the workers studied are unhealthy and that their consumption profile is widely incompatible with the guiding principles of the Food Guide for the Brazilian population. These people are therefore at increased risk of non-transmissible chronic diseases and morbidity and mortality. There is a need to take more effective interventional action, totally restructuring the educational process to form dietary habits, such as implementing public policies targeting this section of the population, which is so important for national development.

The aim of this study is to systematically chart and summarize the literature pertaining to workplace health promotion (WHP) interventions targeting the five main modifiable lifestyle risk factors for chronic disease, including smoking, nutrition, alcohol, physical activity, overweight/obesity (SNAPO) in Australian workers.

The aim of this scoping review was to determine health-related impacts of poor oral health among community-dwelling seniors. Using MeSH terms and keywords such as elderly, general health, geriatrics, 3 electronic databases-Medline, CINAHL, and Age Line were searched. Title and abstracts were independently screened by 3 reviewers, followed by full-texts review. A total of 131 articles met our inclusion criteria, the majority of these studies were prospective cohort (77%, n = 103), and conducted in Japan (42 %, n = 55). These studies were categorized into 16 general health outcomes, with mortality (24%, n = 34), and mental health disorders (21%, n = 30) being the most common outcomes linked with poor oral health. 90% (n = 120) of the included studies reported that poor oral health in seniors can subsequently lead to a higher risk of poor general health outcomes among this population. Improving access to oral healthcare services for elderly can help not only reduce the burden of oral diseases in this population group but also address the morbidity and mortality associated with other general health diseases and conditions caused due to poor oral health. Findings from this study can help identify shortcomings in existing oral healthcare programs for elderly and develop future programs and services to improve access and utilization of oral care services by elderly.