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Journal articles on the topic 'Nutrient-gene interaction'

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Published: 9 March 2023
Last updated: 10 March 2023

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1

López-Carrillo*, Lizbeth, Aubrey V. Herrera, R. Ulises Hernández-Ramirez, Walter Klimecki, A. Jay Gandolfi, and Mariano E. Cebrián. "Nutrient-Gene Interaction in Arsenic Metabolism." ISEE Conference Abstracts 2014, no. 1 (October 20, 2014): 2026. http://dx.doi.org/10.1289/isee.2014.p3-767.

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2

Lee, Wai-Nang P., and Vay Liang W. Go. "Nutrient-Gene Interaction: Tracer-Based Metabolomics." Journal of Nutrition 135, no. 12 (December 1, 2005): 3027S—3032S. http://dx.doi.org/10.1093/jn/135.12.3027s.

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3

Go, Vay Liang W., Christine T. H. Nguyen, Diane M. Harris, and Wai-Nang Paul Lee. "Nutrient-Gene Interaction: Metabolic Genotype-Phenotype Relationship." Journal of Nutrition 135, no. 12 (December 1, 2005): 3016S—3020S. http://dx.doi.org/10.1093/jn/135.12.3016s.

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4

Mocchegiani, Eugenio, Laura Costarelli, Robertina Giacconi, Catia Cipriano, Elisa Muti, Silvia Tesei, and Marco Malavolta. "Nutrient–gene interaction in ageing and successful ageing." Mechanisms of Ageing and Development 127, no. 6 (June 2006): 517–25. http://dx.doi.org/10.1016/j.mad.2006.01.010.

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5

Smith, Daniel L., Crystal H. Maharrey, Christopher R. Carey, Richard A. White, and John L. Hartman. "Gene-nutrient interaction markedly influences yeast chronological lifespan." Experimental Gerontology 86 (December 2016): 113–23. http://dx.doi.org/10.1016/j.exger.2016.04.012.

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6

Vainio, Harri. "Modification of lung cancer prevention by gene-nutrient interaction." Scandinavian Journal of Work, Environment & Health 26, no. 6 (December 2000): 459–60. http://dx.doi.org/10.5271/sjweh.568.

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7

Luan, J. 'a, P. O. Browne, A. H. Harding, D. J. Halsall, S. O'Rahilly, V. K. K. Chatterjee, and N. J. Wareham. "Evidence for Gene-Nutrient Interaction at the PPAR Locus." Diabetes 50, no. 3 (March 1, 2001): 686–89. http://dx.doi.org/10.2337/diabetes.50.3.686.

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8

Reece, Richard J., Laila Beynon, Stacey Holden, Amanda D. Hughes, Karine Rébora, and Christopher A. Sellick. "Nutrient-regulated gene expression in eukaryotes." Biochemical Society Symposia 73 (January 1, 2006): 85–96. http://dx.doi.org/10.1042/bss0730085.

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The recognition of changes in environmental conditions, and the ability to adapt to these changes, is essential for the viability of cells. There are numerous well characterized systems by which the presence or absence of an individual metabolite may be recognized by a cell. However, the recognition of a metabolite is just one step in a process that often results in changes in the expression of whole sets of genes required to respond to that metabolite. In higher eukaryotes, the signalling pathway between metabolite recognition and transcriptional control can be complex. Recent evidence from the relatively simple eukaryote yeast suggests that complex signalling pathways may be circumvented through the direct interaction between individual metabolites and regulators of RNA polymerase II-mediated transcription. Biochemical and structural analyses are beginning to unravel these elegant genetic control elements.
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9

Shirazi-Beechey, S. P., G. A. Allison, I. S. Wood, and J. Dyer. "NUTRIENT AND SUGAR TRANSPORTER GENE INTERACTION IN THE INTESTINAL EPITHELIA." Biochemical Society Transactions 25, no. 3 (August 1, 1997): 459S. http://dx.doi.org/10.1042/bst025459sd.

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10

Rubin, Jill, and Lars Berglund. "Apolipoprotein E and diets: a case of gene-nutrient interaction?" Current Opinion in Lipidology 13, no. 1 (February 2002): 25–32. http://dx.doi.org/10.1097/00041433-200202000-00005.

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11

Zhuang, Pan, Xiaohui Liu, Yin Li, Haoyu Li, Lange Zhang, Xuzhi Wan, Yuqi Wu, Yu Zhang, and Jingjing Jiao. "Circulating Fatty Acids and Genetic Predisposition to Type 2 Diabetes: Gene-Nutrient Interaction Analysis." Diabetes Care 45, no. 3 (January 28, 2022): 564–75. http://dx.doi.org/10.2337/dc21-2048.

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OBJECTIVE To assess the relationship of circulating fatty acids (FA) with risk of type 2 diabetes (T2D) and potential interactions with genetic risk. RESEARCH DESIGN AND METHODS A total of 95,854 participants with complete data on plasma FA from the UK Biobank were enrolled between 2006 and 2010 and were followed up to the end of 2020. Plasma concentrations of saturated fatty acids (SFA), monounsaturated fatty acids (MUFA), and polyunsaturated fatty acids (PUFA) were analyzed by a high-throughput nuclear magnetic resonance–based biomarker profiling platform. The genetic risk scores (GRS) were calculated on the basis of 424 variants associated with T2D. Pathway-specific GRS were calculated based on robust clusters of T2D loci. RESULTS There were 3,052 instances of T2D documented after an average follow-up of 11.6 years. Plasma concentrations of SFA and MUFA were positively associated with T2D risk, while plasma PUFA were inversely associated. After adjustment for major risk factors, hazard ratios (95% CI) of T2D for 1-SD increment were 1.03 (1.02–1.04) for SFA, 1.03 (1.02–1.05) for MUFA, 0.62 (0.56–0.68) for PUFA, 0.67 (0.61–0.73) for n-6 PUFA, 0.90 (0.85–0.95) for n-3 PUFA, and 1.01 (0.98–1.04) for n-6–to–n-3 ratio. Plasma MUFA had significant interactions with the overall GRS and GRS for proinsulin and liver/lipid clusters on T2D risk. The protective associations of n-3 PUFA with T2D risk were weaker among individuals with higher obesity GRS (P interaction = 0.040) and liver/lipid GRS (P interaction = 0.012). Additionally, increased plasma n-3 PUFA concentration was associated with more reductions in T2D risk among participants carrying more docosapentaenoic acid–associated alleles (P interaction = 0.007). CONCLUSIONS Plasma concentrations of SFA and MUFA were associated with a higher T2D risk, whereas plasma PUFA and n-6 and n-3 PUFA were related to a lower risk. Circulating MUFA and n-3 PUFA had significant interactions with genetic predisposition to T2D and FA-associated variants.
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12

Hou, Tim Y., Laurie A. Davidson, Eunjoo Kim, Yang-Yi Fan, Natividad R. Fuentes, Karen Triff, and Robert S. Chapkin. "Nutrient-Gene Interaction in Colon Cancer, from the Membrane to Cellular Physiology." Annual Review of Nutrition 36, no. 1 (July 17, 2016): 543–70. http://dx.doi.org/10.1146/annurev-nutr-071715-051039.

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13

Hesketh, John E., M. Helena Vasconcelos, and Giovanna Bermano. "Regulatory signals in messenger RNA: determinants of nutrient–gene interaction and metabolic compartmentation." British Journal of Nutrition 80, no. 4 (October 1998): 307–21. http://dx.doi.org/10.1017/s0007114598001378.

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Nutrition has marked influences on gene expression and an understanding of the interaction between nutrients and gene expression is important in order to provide a basis for determining the nutritional requirements on an individual basis. The effects of nutrition can be exerted at many stages between transcription of the genetic sequence and production of a functional protein. This review focuses on the role of post-transcriptional control, particularly mRNA stability, translation and localization, in the interactions of nutrients with gene expression. The effects of both macronutrients and micronutrients on regulation of gene expression by post-transcriptional mechanisms are presented and the post-transcriptional regulation of specific genes of nutritional relevance (glucose transporters, transferrin, selenoenzymes, metallothionein, lipoproteins) is described in detail. The function of the regulatory signals in the untranslated regions of the mRNA is highlighted in relation to control of mRNA stability, translation and localization and the importance of these mRNA regions to regulation by nutrients is illustrated by reference to specific examples. The localization of mRNA by signals in the untranslated regions and its function in the spatial organization of protein synthesis is described; the potential of such mechanisms to play a key part in nutrient channelling and metabolic compartmentation is discussed. It is concluded that nutrients can influence gene expression through control of the regulatory signals in these untranslated regions and that the post-transcriptional regulation of gene expression by these mechanisms may influence nutritional requirements. It is emphasized that in studies of nutritional control of gene expression it is important not to focus only on regulation through gene promoters but also to consider the possibility of post-transcriptional control.
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14

Brahe, Lena K., Lars Ängquist, Lesli H. Larsen, Karani S. Vimaleswaran, Jörg Hager, Nathalie Viguerie, Ruth J. F. Loos, et al. "Influence of SNPs in nutrient-sensitive candidate genes and gene–diet interactions on blood lipids: the DiOGenes study." British Journal of Nutrition 110, no. 5 (January 29, 2013): 790–96. http://dx.doi.org/10.1017/s0007114512006058.

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Blood lipid response to a given dietary intervention could be determined by the effect of diet, gene variants or gene–diet interactions. The objective of the present study was to investigate whether variants in presumed nutrient-sensitive genes involved in lipid metabolism modified lipid profile after weight loss and in response to a given diet, among overweight European adults participating in the Diet Obesity and Genes study. By multiple linear regressions, 240 SNPs in twenty-four candidate genes were investigated for SNP main and SNP–diet interaction effects on total cholesterol, LDL-cholesterol, HDL-cholesterol and TAG after an 8-week low-energy diet (only main effect), and a 6-monthad libitumweight maintenance diet, with different contents of dietary protein or glycaemic index. After adjusting for multiple testing, a SNP–dietary protein interaction effect on TAG was identified for lipin 1 (LPIN1) rs4315495, with a decrease in TAG of − 0·26 mmol/l per A-allele/protein unit (95 % CI − 0·38, − 0·14,P= 0·000043). In conclusion, we investigated SNP–diet interactions for blood lipid profiles for 240 SNPs in twenty-four candidate genes, selected for their involvement in lipid metabolism pathways, and identified one significant interaction betweenLPIN1rs4315495 and dietary protein for TAG concentration.
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15

Hesketh, J. E., M. H. Vasconcelos, and G. Bermano. "Regulatory signals in messenger RNA: determinants of nutrient-gene interaction and metabolic compartmentation." British Journal Of Nutrition 80, no. 4 (October 1, 1998): 307–21. http://dx.doi.org/10.1079/096582198388265.

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16

Suominen, A. H., D. R. Glimm, D. Tedesco, E. K. Okine, M. I. McBurney, and J. J. Kennelly. "Intestinal nutrient-gene interaction: the effect of feed deprivation and refeeding on cholecystokinin and proglucagon gene expression." Journal of Animal Science 76, no. 12 (1998): 3104. http://dx.doi.org/10.2527/1998.76123104x.

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17

Ordovas, J. M. "Gene-diet interaction and plasma lipid responses to dietary intervention." Biochemical Society Transactions 30, no. 2 (April 1, 2002): 68–73. http://dx.doi.org/10.1042/bst0300068.

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Strategies for disease prevention can have a major impact on people's health. However, major gaps exist in our knowledge with regard to nutritional adequacy, nutrient-disease interactions, nutrient-gene interactions, and effective strategies for implementation of dietary recommendations which have the potential to decrease the disease burden and to contribute to successful aging of the population. Coronary heart disease is one of the major causes of mortality in the world. We have sound evidence that high levels of low-density lipoprotein cholesterol (LDL-C) and low levels of high-density lipoprotein cholesterol (HDL-C) are associated with increased risk of coronary heart disease. Lipoprotein concentrations are associated with environmental variables such as diet and lifestyle, but genetics also play a significant role. We have examined polymorphisms at candidate loci to determine their usefulness as markers for dietary responses. A G/A polymorphism 75 bp upstream from the gene encoding apolipoprotein AI (APOA1) has been described in ~ 30% of the population. Our studies show that this polymorphism is associated with variability in the HDL-C response to dietary fat, specifically to polyunsaturated fatty acids (PUFA) in the diet. Carriers of the A allele respond to increases in dietary PUFA with elevations in HDL-C levels, probably due to altered interactions of transcription factors with the mutated promoter. Therefore carriers of the A allele can potentially decrease their atherogenic risk by consuming high-PUFA diets. Likewise, we have examined the interaction between other dietary habits, such as alcohol drinking, and variability at the APOE locus, and have demonstrated that the classical associations between APOE polymorphism and LDL-C levels are observed primarily in those subjects who consume alcohol. Moreover, we have found a subgroup of the population, APOE4 carriers, for whom drinking alcohol may exert detrimental effects on lipid metabolism. This knowledge will contribute towards the development of more effective personalized dietary recommendations.
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18

Howard, Susie C., Ya-Wen Chang, Yelena V. Budovskaya, and Paul K. Herman. "The Ras/PKA Signaling Pathway of Saccharomyces cerevisiae Exhibits a Functional Interaction With the Sin4p Complex of the RNA Polymerase II Holoenzyme." Genetics 159, no. 1 (September 1, 2001): 77–89. http://dx.doi.org/10.1093/genetics/159.1.77.

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Abstract Saccharomyces cerevisiae cells enter into the G0-like resting state, stationary phase, in response to specific types of nutrient limitation. We have initiated a genetic analysis of this resting state and have identified a collection of rye mutants that exhibit a defective transcriptional response to nutrient deprivation. These transcriptional defects appear to disrupt the control of normal growth because the rye mutants are unable to enter into a normal stationary phase upon nutrient deprivation. In this study, we examined the mutants in the rye1 complementation group and found that rye1 mutants were also defective for stationary phase entry. Interestingly, the RYE1 gene was found to be identical to SIN4, a gene that encodes a component of the yeast Mediator complex within the RNA polymerase II holoenzyme. Moreover, mutations that affected proteins within the Sin4p module of the Mediator exhibited specific genetic interactions with the Ras protein signaling pathway. For example, mutations that elevated the levels of Ras signaling, like RAS2val19, were synthetic lethal with sin4. In all, our data suggest that specific proteins within the RNA polymerase II holoenzyme might be targets of signal transduction pathways that are responsible for coordinating gene expression with cell growth.
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19

Long, Kendall J., Chanel A. Mosby, and Melissa K. Jones. "Glucose Reduces Norovirus Binding to Enterobacter cloacae and Alters Gene Expression of Bacterial Surface Structures in a Growth Phase Dependent Manner." Viruses 14, no. 8 (July 22, 2022): 1596. http://dx.doi.org/10.3390/v14081596.

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Norovirus is the leading cause of acute viral gastroenteritis. Both human and murine noroviruses attach to commensal bacteria belonging to the mammalian gut flora, and binding levels are influenced by nutrients present in bacterial media. However, it is not known which nutrients are responsible for altering viral binding or why binding is altered. Gene expression of commensal bacteria can be changed by the external environment as well as by interaction with pathogens. For example, growth phase and incubation conditions impact expression levels of specific bacterial genes in Escherichia coli. We have previously shown that binding by both human and murine noroviruses to the commensal bacterium Enterobacter cloacae induces genome-wide changes in gene expression with a large number of differentially expressed genes associated with the surface structure of the bacterial cell. The current study evaluated norovirus binding under nutrient-limited conditions and assessed the expression of a select panel of these genes that are significantly altered by norovirus binding under these conditions. The goal of this work was to determine how norovirus attachment to Enterobacter cloacae affected the expression of these genes under varying nutrient and growth phase conditions. We found that the presence of glucose in minimal media reduced murine norovirus binding to E. cloacae and viral binding in the presence of glucose reduced gene expression for surface structures previously associated with norovirus attachment. Changes in viral binding and gene expression occurred in a growth phase-dependent manner. Collectively, these data demonstrate that both the growth phase and nutrient availability alter viral interactions with commensal bacteria and the subsequent changes in gene expression. Ultimately, this work advances our understanding of norovirus-bacterium interactions and provides a foundation for elucidating the conditions and surface structures that regulate norovirus attachment to bacteria.
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20

Bousquet-Moore, Danielle, Richard E. Mains, and Betty A. Eipper. "Peptidylgycine α-amidating monooxygenase and copper: A gene-nutrient interaction critical to nervous system function." Journal of Neuroscience Research 88, no. 12 (April 9, 2010): 2535–45. http://dx.doi.org/10.1002/jnr.22404.

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21

Bickerstaffe, R. "Regulation of nutrient partitioning growth and lactation." Australian Journal of Agricultural Research 44, no. 3 (1993): 523. http://dx.doi.org/10.1071/ar9930523.

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This paper will emphasize the impact of growth and lactation on partitioning nutrients, the role of biological signals and whether such signals can be influenced or modified. Factors considered are the mechanisms of controlling cell cycling, growth and differentiation; interaction or cross-talking between tissues (autocrinepeptides, tissue receptors, secondary messengers); effect of extrinsic and intrinsic signals on cellular growth (growth hormones, oncogenes); and manipulation of nutrient partitioning (mutated receptors, gene expression, targeting metabolic genes).
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22

He, Dan, Yuanyuan Liu, Qinglong L. Wu, Yuyang Peng, and Lijuan Ren. "Humic Lake Exhibits Higher Microbial Functional Gene Diversity and Weaker Gene Interaction Efficiency than a Common Alkaline Lake." Biology 11, no. 10 (October 1, 2022): 1448. http://dx.doi.org/10.3390/biology11101448.

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Humic lakes (HLs) are special water bodies (high organic matter content, low pH, and low transparency) that are important sources of major greenhouse gases. The knowledge about microbial functional potentials and the interactions among different genes in HL water has been scarcely understood. In this study, we used 16S rRNA gene sequencing and the GeoChip 5.0 to investigate microbial community compositions and functional gene structures in an HL and a reference weakly alkaline lake (RAL). The HL microbial communities showed distinct compositions and functional gene structures than those in the RAL. The functional gene diversity was significantly higher in the HL than in the RAL. Specifically, higher gene relative intensities in carbon and nitrogen fixations, the degradation of various types of carbon, methane oxidation and methanogenesis, ammonification, denitrification, and assimilatory N reduction were observed in the HL samples. By contrast, the metabolic potentials of microorganisms involved in dissimilatory N reduction, phosphorus degradation, and sulfur oxidation were weaker in the HL than in the RAL. Despite higher functional gene diversity, the interaction efficiency among genes (reflected by network geodesic distance and clustering coefficient) might be reduced in the HL. Different functional microbes may develop less interdependent relationships in acquiring nutrients given the high resource availability in the HL. Overall, the enhanced microbial metabolic potentials and less efficient functional interactions might have great consequences on nutrient cycling and greenhouse gas emissions in the HL ecosystem.
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23

Halloum, Iman, Houssein Al-Attrache, Katia El-Ghoz, Lara Hammoud, and Ziad Abdel-Razzak. "Dose-dependent interaction of two heavy metals with amiodarone toxicity in Saccharomyces cerevisiae." Toxicology and Industrial Health 38, no. 5 (May 2022): 249–58. http://dx.doi.org/10.1177/07482337221088354.

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Amiodarone (AMD) is an antiarrhythmic drug that induces idiosyncratic toxicity. Environmental pollutants, including heavy metals, could interact with its toxicity by affecting pharmacokinetics and pharmacodynamics. Other levels of interaction could exist in yeast, such as oxidative stress and the general stress response. In this study, we investigated the interaction of mercury chloride (HgCl2) and cadmium chloride (CdCl2) with AMD toxicity on Saccharomyces cerevisiae. Interaction type - synergistic, additive, or antagonistic - was determined by median drug effect analysis using “CompuSyn”. HgCl2 potentiated AMD toxicity at high doses (≥ 71.4 μm, which yielded more than 60% inhibition). CdCl2 acted similarly at high doses (≥ 57.9 μm). An antagonistic effect appeared at lower doses with both heavy metals (≤ 49.4 μm for HgCl2 and AMD; ≤ 18.9 μm for CdCl2 and AMD). The threshold concentrations (HgCl2 or CdCl2 combined with AMD) that switched the interaction from antagonistic to additive, and then to synergistic, were decreased in the yeast strain mutant in catalase ( CTT1), suggesting an important role for this enzyme. Moreover, mutation of the nutrient sensing receptor gene GPR1 caused the synergistic interaction of CdCl2, but not HgCl2, with AMD to occur at the lowest tested concentrations (1.2 μm). The reverse was obtained with the mutant strain in calcium–manganese transporter gene PMR1, where the synergistic interaction of HgCl2 with AMD occurred at concentrations (20.7 μm) lower than that of the wild type (71.4 μm). These results demonstrated a dose-dependent interaction between the two heavy metals with AMD toxicity, and the involvement of oxidative stress, calcium homeostasis, and nutrient sensing in the observed interaction.
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24

Eaton, Carla J., Pierre-Yves Dupont, Peter Solomon, William Clayton, Barry Scott, and Murray P. Cox. "A Core Gene Set Describes the Molecular Basis of Mutualism and Antagonism in Epichloë spp." Molecular Plant-Microbe Interactions® 28, no. 3 (March 2015): 218–31. http://dx.doi.org/10.1094/mpmi-09-14-0293-fi.

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Beneficial plant–fungal interactions play an important role in the ability of plants to survive changing environmental conditions. In contrast, phytopathogenic fungi fall at the opposite end of the symbiotic spectrum, causing reduced host growth or even death. In order to exploit beneficial interactions and prevent pathogenic ones, it is essential to understand the molecular differences underlying these alternative states. The association between the endophyte Epichloë festucae and Lolium perenne (perennial ryegrass) is an excellent system for studying these molecular patterns due to the existence of several fungal mutants that have an antagonistic rather than a mutualistic interaction with the host plant. By comparing gene expression in a wild-type beneficial association with three mutant antagonistic associations disrupted in key signaling genes, we identified a core set of 182 genes that show common differential expression patterns between these two states. These gene expression changes are indicative of a nutrient-starvation response, as supported by the upregulation of genes encoding degradative enzymes, transporters, and primary metabolism, and downregulation of genes encoding putative small-secreted proteins and secondary metabolism. These results suggest that disruption of a mutualistic symbiotic interaction may lead to an elevated uptake and degradation of host-derived nutrients and cell-wall components, reminiscent of phytopathogenic interactions.
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25

Spener, Friedrich. "Adoption of lipid by nuclear receptors– a clear-cut example of a specific nutrient-gene interaction?" European Journal of Lipid Science and Technology 106, no. 7 (July 2004): 403–4. http://dx.doi.org/10.1002/ejlt.200490041.

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26

Haggarty, Paul. "B-vitamins, genotype and disease causality." Proceedings of the Nutrition Society 66, no. 4 (October 25, 2007): 539–47. http://dx.doi.org/10.1017/s0029665107005861.

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Despite a great deal of research effort there is still considerable uncertainty surrounding the importance of the B-vitamins in health and disease. This continuing uncertainty is partly a result of the difficulty of measuring intake, confounding in observational studies and the very large numbers required to evaluate primary prevention in randomised controlled trials. Consequently, genetic data are increasingly being used to infer nutritional effects on health and even in the formulation of nutrition policy using the approach of ‘mendelian randomisation’. Genetic information has already contributed greatly to the understanding of B-vitamin metabolism and the heterogeneity of responses to intake. It has the potential to provide further nutritional insights and to assist in the elucidation of causal mechanisms, but it is important that genetic data is not viewed as an alternative to nutritional information, both are necessary when addressing nutritional problems. Similarly, the interpretation of nutrient and biomarker status in some experimental designs may require knowledge of genotype. Formal tests of gene–gene and gene–nutrient interaction are of limited value in nutritional studies and the formulation of policy. Graphical representation of diet–genotype–health data greatly assists in the elucidation of the nature of genetic effects, their interaction with nutrition and the implications for nutrition policy.
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Hajiluian, Ghazaleh, Mahdieh Abbasalizad Farhangi, and Leila Jahangiry. "Mediterranean dietary pattern and VEGF +405 G/C gene polymorphisms in patients with metabolic syndrome: An aspect of gene-nutrient interaction." PLOS ONE 12, no. 2 (February 17, 2017): e0171637. http://dx.doi.org/10.1371/journal.pone.0171637.

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28

Zheng, Ju-Sheng, Laurence D. Parnell, Caren E. Smith, Yu-Chi Lee, Aziza Jamal-Allial, Yiyi Ma, Duo Li, Katherine L. Tucker, José M. Ordovás, and Chao-Qiang Lai. "Circulating 25-Hydroxyvitamin D, IRS1 Variant rs2943641, and Insulin Resistance: Replication of a Gene–Nutrient Interaction in 4 Populations of Different Ancestries." Clinical Chemistry 60, no. 1 (January 1, 2014): 186–96. http://dx.doi.org/10.1373/clinchem.2013.215251.

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Abstract BACKGROUND Associations of either insulin receptor substrate 1 (IRS1) variants or circulating 25-hydroxyvitamin D [25(OH)D] with type 2 diabetes (T2D) and insulin resistance (IR) are inconsistent. This study sought to determine whether circulating 25(OH)D modulates the association of a potentially functional variant at IRS1 (rs2943641) with insulin resistance. METHOD Interaction between IRS1 rs2943641 and circulating 25(OH)D on homeostasis model assessment for IR (HOMA-IR) was examined in the Boston Puerto Rican Health Study (BPRHS) (n = 1144). Replication was performed in the African-American (n = 1126), non-Hispanic white (n = 1967), and Hispanic (n = 1241) populations of the Multi-Ethnic Study of Atherosclerosis (MESA) with genotypes of 3 IRS1 variants, rs2972144, rs1515104, and rs2673142, which are tag single nucleotide polymorphisms (SNPs) and in strong linkage disequilibrium with rs2943641. RESULTS Higher circulating 25(OH)D was associated with lower risk of T2D and IR in BPRHS women homozygous for minor allele rs2943641T. Consistently, in each of 3 MESA populations, HOMA-IR and insulin decreased more evidently with higher circulating 25(OH)D in women of the rs2943641TT genotype than in carriers of the major allele (rs2943641C). Metaanalysis indicated significant and consistent interactions between circulating 25(OH)D and IRS1 variants on HOMA-IR (log transformed) [pooled β = −0.008, 95% CI: −0.016 to −0.001, P interaction = 0.004] and insulin (log transformed) (pooled β = −0.006, 95% CI: −0.011 to −0.002, P interaction = 0.023) in 3065 women of the 4 populations. CONCLUSIONS Participants with different genotypes of IRS1 rs2943641 exhibit differential benefit from high circulating 25(OH)D for the reduction of insulin resistance and T2D risk. This gene–nutrient interaction, which appears to be limited to women, warrants further examination in randomized controlled trials of vitamin D supplementation.
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Carter, R. Colin, Antonio Di Narzo, Steven Zeisel, Neil Dodge, Ernesta Meintjes, Christopher Molteno, Joseph Jacobson, and Sandra Jacobson. "Choline Metabolism Gene-Exposure Interactions in Fetal Alcohol-related Memory Deficits." Current Developments in Nutrition 6, Supplement_1 (June 2022): 627. http://dx.doi.org/10.1093/cdn/nzac061.011.

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Abstract Objectives Animal and human studies have demonstrated the potential for the essential nutrient choline to ameliorate teratogenic effects of prenatal alcohol exposure (PAE), including growth and recognition memory deficits. We hypothesized that the presence of maternal SNPs in choline metabolism-related genes may modify fetal vulnerability to PAE. Methods Mothers from two prenatally recruited birth cohorts in Cape Town, South Africa (discovery cohort: n = 149; validation cohort: n = 153) were genotyped for 315 SNPs in choline metabolism-related genes. Primary outcomes were: height/length z-scores (disc. at age 9 yr; val. at 5 yr) and recognition memory (disc. = CVLT-C recognition discrimination score, age 9 yr; val. = Fagan Test of Infant Intelligence novelty preference score, 6.5 and 12 mo). Linear regression models were constructed using OLS: outcome ∼ PAE + gene dose (# effective alleles) + PAE x gene dose; significance of PAE-gene interaction was tested using a 2-sided Wald test on the PAE-gene dose interaction term with Benjamini-Hochberg (BH) multiple testing correction. Results PAE (drinking days/wk) was related to shorter height (disc. B(95% CI) = −.11(−.18, −.01); val. B = −.12(−.20, −.04) and poorer recognition memory (disc. B = −.11(−.26, −.02); val. B = −.11(−.19, −.03)). Gene-PAE interaction for recognition memory was seen in both cohorts for rs12262538 (discovery BH-adj. p = .0015; validation unadj. p = .004); for rs1043261, discovery BH-adj. p = .0235 and validation unadj. p = .0903. No gene-PAE interactions were seen for height. rs12262538 is in the 5’ flanking region near the Stearoyl-CoA Desaturase (SCD) gene. rs1043261 is in the 3’ flanking region near the choline dehydrogenase (CHDH) gene. Conclusions We identified two maternal SNPs that may confer higher fetal risk for teratogenic effects of PAE. These findings support the potential protective role of choline in fetal alcohol spectrum disorders prevention. Funding Sources National Institute on Alcohol Abuse and Alcoholism.
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Vimaleswaran, Karani S. "A nutrigenetics approach to study the impact of genetic and lifestyle factors on cardiometabolic traits in various ethnic groups: findings from the GeNuIne Collaboration." Proceedings of the Nutrition Society 79, no. 2 (January 31, 2020): 194–204. http://dx.doi.org/10.1017/s0029665119001186.

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Several studies on gene–diet interactions (nutrigenetics) have been performed in western populations; however, there are only a few studies to date in lower middle-income countries (LMIC). A large-scale collaborative project called gene–nutrient interactions (GeNuIne) Collaboration, the main objective of which is to investigate the effect of GeNuIne on cardiometabolic traits using population-based studies from various ethnic groups, has been initiated at the University of Reading, UK. While South Asians with higher genetic risk score (GRS) showed a higher risk of obesity in response to a high-carbohydrate diet, South East and Western Asian populations with higher GRS showed an increased risk of central obesity in response to a high-protein diet. The paper also provides a summary of other gene–diet interaction analyses that were performed in LMIC as part of this collaborative project and gives an overview of how these nutrigenetic findings can be translated to personalised and public health approaches for the prevention of cardiometabolic diseases such as obesity, type 2 diabetes and CVD.
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Wang, Zhiquan, Longjie Ni, Liangqin Liu, Haiyan Yuan, Suzhen Huang, and Chunsun Gu. "Screening and Identification of Host Proteins Interacting with Iris lactea var. chinensis Metallothionein IlMT2a by Yeast Two-Hybrid Assay." Genes 12, no. 4 (April 10, 2021): 554. http://dx.doi.org/10.3390/genes12040554.

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Iris lactea var. chinensis (Fisch.) (I. lactea var. chinensis) is a well-known cadmium (Cd)-tolerant plant and we have previously shown that the metallothionein gene, IlMT2a, of the plant may be playing a key role in conferring the Cd tolerance. In this study, we have identified several proteins interacting with the IlMT2a by screening yeast two-hybrid library constructed from cDNAs isolated from Cd-treated I. lacteal var. chinensis plants. Putative functions of these proteins include those involved in photosynthesis, ROS scavenge, nutrient transport, and transcriptional regulation, to name a few. In particular, another metallothionein, which we assigned the name of IlMT3, was identified as an interacting partner of the IlMT2a. Unlike IlMT2a, it did not provide any significant protection against Cd toxicity in transgenic Arabidopsis thaliana L. (A. thaliana). To our knowledge, this is the first time ever reporting the interaction of two metallothionein proteins in plants. Learning the biological significance of the interaction between IlMT2a and IlMT3 would be the focus of future study and would be able to provide valuable insights into the understanding plant metallothionein’s diverse and complex roles in coordinating many important cellular physiologies including stress responses, gene regulations, and energy metabolisms.
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Scrimshaw, Nevin S. "Viewing Disease as the Synergistic Interaction of Host, Agent, and Environment." Food and Nutrition Bulletin 16, no. 3 (September 1995): 1–6. http://dx.doi.org/10.1177/156482659501600305.

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The agent of disease, whether it is an infectious organism, the deficiency or excess of a nutrient, a toxin, or the expression of a gene, is not sufficient to explain its cause. The impact of the agent depends on host factors and the influence of physical, biological, and social factors in the environment. For nutritional disorders those of the social environment, including the complex of educational, economic, religious, political, and other factors, are likely to be the most important and also the most difficult to understand and modify. If nutritional and other diseases are viewed as problems in human ecology, the primary health-care approach to their prevention follows naturally.
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CHOI, Jeong-hwa, Zoe YATES, Charlotte MARTIN, Lyndell BOYD, Xiaowei NG, Virginia SKINNER, Ron WAI, Martin VEYSEY, and Mark LUCOCK. "Gene-Nutrient Interaction between Folate and Dihydrofolate Reductase in Risk for Adenomatous Polyp Occurrence: A Preliminary Report." Journal of Nutritional Science and Vitaminology 61, no. 6 (2015): 455–59. http://dx.doi.org/10.3177/jnsv.61.455.

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Martínez-Hernández, Alfredo, Luís Enríquez, María Jesús Moreno-Moreno, and Amelia Martí. "Genetics of obesity." Public Health Nutrition 10, no. 10A (October 2007): 1138–44. http://dx.doi.org/10.1017/s1368980007000626.

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AbstractObjectiveThe aim was to review and update advances in genetics of obesity.DesignAnalysis and interpretation of recent investigations about regulating the energy balance as well as about gene-nutrient interactions and current nutrigenomic research methods.Background and main statementsObesity results from a long-term positive energy balance. However, its rising prevalence in developed and developing societies must reflect lifestyle changes, since genetic susceptibility remains stable over many generations. Like most complex diseases, obesity derives from a failure of adequate homoeostasis within the physiological system controlling body weight. The identification of genes that are involved in syndromic, monogenic and polygenic obesity has seriously improved our knowledge of body weight regulation. This disorder may arise from a deregulation at the genetic level (e.g. gene transcription or altered protein function) or environmental exposure (e.g. diet, physical activity, etc.).ConclusionsIn practice, obesity involves the interaction between genetic and environmental factors.
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Xie, Xianan, Xiaoning Fan, Hui Chen, and Ming Tang. "Phosphorus Starvation- and Zinc Excess-Induced Astragalus sinicus AsZIP2 Zinc Transporter Is Suppressed by Arbuscular Mycorrhizal Symbiosis." Journal of Fungi 7, no. 11 (October 22, 2021): 892. http://dx.doi.org/10.3390/jof7110892.

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Zinc (Zn) is one of the most essential micronutrients for plant growth and metabolism, but Zn excess can impair many basic metabolic processes in plant cells. In agriculture, crops often experience low phosphate (Pi) and high Zn double nutrient stresses because of inordinate agro-industrial activities, while the dual benefit of arbuscular mycorrhizal (AM) fungi protects plants from experiencing both deficient and toxic nutrient stresses. Although crosstalk between Pi and Zn nutrients in plants have been extensively studied at the physiological level, the molecular basis of how Pi starvation triggers Zn over-accumulation in plants and how AM plants coordinately modulate the Pi and Zn nutrient homeostasis remains to be elucidated. Here, we report that a novel AsZIP2 gene, a Chinese milk vetch (Astragalus sinicus) member of the ZIP gene family, participates in the interaction between Pi and Zn nutrient homeostasis in plants. Phylogenetic analysis revealed that this AsZIP2 protein was closely related to the orthologous Medicago MtZIP2 and Arabidopsis AtZIP2 transporters. Gene expression analysis indicated that AsZIP2 was highly induced in roots by Pi starvation or Zn excess yet attenuated by arbuscular mycorrhization in a Pi-dependent manner. Subcellular localization and heterologous expression experiments further showed that AsZIP2 encoded a functional plasma membrane-localized transporter that mediated Zn uptake in yeast. Moreover, overexpression of AsZIP2 in A. sinicus resulted in the over-accumulation of Zn concentration in roots at low Pi or excessive Zn concentrations, whereas AsZIP2 silencing lines displayed an even more reduced Zn concentration than control lines under such conditions. Our results reveal that the AsZIP2 transporter functioned in Zn over-accumulation in roots during Pi starvation or high Zn supply but was repressed by AM symbiosis in a Pi-dependent manner. These findings also provide new insights into the AsZIP2 gene acting in the regulation of Zn homeostasis in mycorrhizal plants through Pi signal.
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Ward, Mandy J., Helen Lew, Anke Treuner-Lange, and David R. Zusman. "Regulation of Motility Behavior in Myxococcus xanthus May Require an Extracytoplasmic-Function Sigma Factor." Journal of Bacteriology 180, no. 21 (November 1, 1998): 5668–75. http://dx.doi.org/10.1128/jb.180.21.5668-5675.1998.

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ABSTRACT Using interaction trap technology, we identified a putative extracytoplasmic-function (ECF) sigma factor (RpoE1) inMyxococcus xanthus, a bacterium which has a complex life cycle that includes fruiting body formation. The first domain of the response regulator protein FrzZ, a component of the Frz signal transduction system, was used as bait. Although the RpoE1 protein displayed no interactions with control proteins presented as bait, a weak interaction with a second M. xanthus response regulator (AsgA) was observed. While the specificity of the FrzZ-RpoE1 interaction therefore remains speculative, cloning and sequencing of the region surrounding rpoE1 localized it to a position downstream of the frzZ gene. A potential promoter site for binding of an ECF sigma factor was identified upstream ofrpoE1, suggesting the gene may be autoregulated. However, primer extension studies suggested that transcription ofrpoE1 occurs under both vegetative and developmental conditions from a ς70-like promoter. Dot blot analysis of RNA preparations confirmed the low-level, constitutive expression ofrpoE1 during both stages of the life cycle. Analysis of an insertion mutant also indicated a role for RpoE1 under both vegetative and developmental conditions, since swarming was reduced on nutrient-rich agar and developmental aggregation was effected under starvation conditions, especially at high cell densities. An insertion mutation introduced into the gene directly downstream ofrpoE1 (orf5) did not result in either swarming or developmental aggregation defects, even though the gene is transcribed as part of the same operon. Therefore, we propose that this new ECF sigma factor could play a role in the transcriptional regulation of genes involved in motility behavior during both stages of the complex M. xanthus life cycle.
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Stubbs, AK, NM Wheelhouse, MA Lomax, and DG Hazlerigg. "Nutrient-hormone interaction in the ovine liver: methionine supply selectively modulates growth hormone-induced IGF-I gene expression." Journal of Endocrinology 174, no. 2 (August 1, 2002): 335–41. http://dx.doi.org/10.1677/joe.0.1740335.

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This study tested the hypothesis that specific amino acids are responsible for modulating the insulin-like growth factor-I (IGF-I) response to growth hormone (GH) in ovine hepatocytes. Cells were grown in media of defined amino acid composition, based on physiological concentrations (P.C.) of amino acids in sheep plasma. Relative to culture in 5 x P.C., amino acid limitation to 0.2 x P.C. had inhibitory effects on IGF-I RNA expression, peptide release and p70 S6 kinase phosphorylation (P<0.01 in each case). Limitation of methionine levels to 0.2 x P.C. against a background of 5 x P.C. for the other amino acids blocked GH-stimulated IGF-I peptide release and RNA expression, although basal expression was unaffected. In contrast, limitation of the other amino acids present in the culture medium had no effect on basal or GH-stimulated IGF-I expression. Selective methionine limitation to 0.2xP.C. levels had no effect on cellular or secretory protein synthesis rates relative to cells grown in complete 5 x P.C. medium but did cause a partial reduction in p70 S6 kinase phosphorylation, which was also observed when medium was selectively limited for other essential amino acids. The addition of rapamycin (5 ng/ml) to cells grown in 5xP.C. media completely abolished p70 S6 kinase phosphorylation (P<0.001), implicating mTOR in the response of S6 kinase phosphorylation to changing amino acid supply. By contrast, inclusion of rapamycin (100 ng/ml) had no effect on levels of IGF-I gene expression. These results indicate that methionine is the key limiting amino acid involved in the modulation of IGF-I expression in the ovine liver. This nutrient-hormone interaction is a highly selective phenomenon, occurring against a background of modest effects on general protein synthetic control. The partial inhibitory effects of methionine on mTOR activity are not sufficient to account for this selectivity of action.
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Li, Qian, Qing Lan, Yawei Zhang, Bryan A. Bassig, Theodore R. Holford, Brian Leaderer, Peter Boyle, et al. "Role of one-carbon metabolizing pathway genes and gene–nutrient interaction in the risk of non-Hodgkin lymphoma." Cancer Causes & Control 24, no. 10 (August 3, 2013): 1875–84. http://dx.doi.org/10.1007/s10552-013-0264-3.

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Akinyele, Oluwaseun, and Heather M. Wallace. "Understanding the Polyamine and mTOR Pathway Interaction in Breast Cancer Cell Growth." Medical Sciences 10, no. 3 (September 10, 2022): 51. http://dx.doi.org/10.3390/medsci10030051.

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The polyamines putrescine, spermidine and spermine are nutrient-like polycationic molecules involved in metabolic processes and signaling pathways linked to cell growth and cancer. One important pathway is the PI3K/Akt pathway where studies have shown that polyamines mediate downstream growth effects. Downstream of PI3K/Akt is the mTOR signaling pathway, a nutrient-sensing pathway that regulate translation initiation through 4EBP1 and p70S6K phosphorylation and, along with the PI3K/Akt, is frequently dysregulated in breast cancer. In this study, we investigated the effect of intracellular polyamine modulation on mTORC1 downstream protein and general translation state in two breast cancer cell lines, MCF-7 and MDA-MB-231. The effect of mTORC1 pathway inhibition on the growth and intracellular polyamines was also measured. Results showed that polyamine modulation alters 4EBP1 and p70S6K phosphorylation and translation initiation in the breast cancer cells. mTOR siRNA gene knockdown also inhibited cell growth and decreased putrescine and spermidine content. Co-treatment of inhibitors of polyamine biosynthesis and mTORC1 pathway induced greater cytotoxicity and translation inhibition in the breast cancer cells. Taken together, these data suggest that polyamines promote cell growth in part through interaction with mTOR pathway. Similarly intracellular polyamine content appears to be linked to mTOR pathway regulation. Finally, dual inhibition of polyamine and mTOR pathways may provide therapeutic benefits in some breast cancers.
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Hoke, Alexa K., Guadalupe Reynoso, Morgan R. Smith, Malia I. Gardner, Dominique J. Lockwood, Naomi E. Gilbert, Steven W. Wilhelm, et al. "Genomic signatures of Lake Erie bacteria suggest interaction in the Microcystis phycosphere." PLOS ONE 16, no. 9 (September 22, 2021): e0257017. http://dx.doi.org/10.1371/journal.pone.0257017.

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Microbial interactions in harmful algal bloom (HAB) communities have been examined in marine systems, but are poorly studied in fresh waters. To investigate HAB-microbe interactions, we isolated bacteria with close associations to bloom-forming cyanobacteria, Microcystis spp., during a 2017 bloom in the western basin of Lake Erie. The genomes of five isolates (Exiguobacterium sp. JMULE1, Enterobacter sp. JMULE2, Deinococcus sp. JMULE3, Paenibacillus sp. JMULE4, and Acidovorax sp. JMULE5.) were sequenced on a PacBio Sequel system. These genomes ranged in size from 3.1 Mbp (Exiguobacterium sp. JMULE1) to 5.7 Mbp (Enterobacter sp. JMULE2). The genomes were analyzed for genes relating to critical metabolic functions, including nitrogen reduction and carbon utilization. All five of the sequenced genomes contained genes that could be used in potential signaling and nutrient exchange between the bacteria and cyanobacteria such as Microcystis. Gene expression signatures of algal-derived carbon utilization for two isolates were identified in Microcystis blooms in Lake Erie and Lake Tai (Taihu) at low levels, suggesting these organisms are active and may have a functional role during Microcystis blooms in aggregates, but were largely missing from whole water samples. These findings build on the growing evidence that the bacterial microbiome associated with bloom-forming algae have the functional potential to contribute to nutrient exchange within bloom communities and interact with important bloom formers like Microcystis.
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Singh, Parul, Natalia Kunz, Gaelle Le Friec, Luopin Wang, Paul Lavender, Majid Kazemian, and Claudia Kemper. "A novel and human-specific CD46-KLF/SP interaction mediates gene expression required for successful Th1 induction." Journal of Immunology 204, no. 1_Supplement (May 1, 2020): 76.13. http://dx.doi.org/10.4049/jimmunol.204.supp.76.13.

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Abstract Signals mediated by autocrine activation of the human-specific complement receptor CD46 during T cell receptor (TCR) stimulation are vital to Th1 induction in human CD4+ T cells, but how exactly CD46 in a molecular level mediates this role is currently undefined. CD46 is expressed in different isoforms that can bear either one of two distinct cytoplasmic tails: CYT-1 or CYT-2. Nuclear translocation of CYT-1 is a critical requirement for the expression of genes coding for nutrient-influx-channels and mTORC1 activity that mediate metabolic adaptations needed for Th1 responses. The lack of a DNA binding domain in CD46-CYT-1 precludes it from acting directly as a transcription factor (TF) and we hence hypothesized that CYT-1 regulates gene expression via direct interaction with specific TF activator and/or repressor complexes. Indeed, CUT&RUN experiments performed using our novel antibody raised against cleaved CYT-1 identified key members of the KLF/SP TFs gene family as potential interacting partners of CD46-CYT-1. Subsequent ELISA and MST experiment confirmed strong, dose-dependent CYT-1/KLF/SP TFs interactions and also demonstrated that CYT-1 fostered KLF/SP TFs binding to appropriate DNA motifs. Genome-wide comparison of the KLF/SP TFs and CYT1 bound genes in T cells revealed their enrichment in crucial basic cell-physiological pathways. Moreover, the CUT&RUN data in conjunction with ATAC-seq analyses indicated that this novel CYT-1/KLF/SP axis may control general chromatin remodeling – a notion we are currently exploring. These data define a novel and critical human-specific pathway of gene regulation and further underpin the vital role of intracellular/autocrine complement in the regulation of normal cellular activity.
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Jamsheer K, Muhammed, Manoj Kumar, and Vibha Srivastava. "SNF1-related protein kinase 1: the many-faced signaling hub regulating developmental plasticity in plants." Journal of Experimental Botany 72, no. 17 (March 8, 2021): 6042–65. http://dx.doi.org/10.1093/jxb/erab079.

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Abstract The Snf1-related protein kinase 1 (SnRK1) is the plant homolog of the heterotrimeric AMP-activated protein kinase/sucrose non-fermenting 1 (AMPK/Snf1), which works as a major regulator of growth under nutrient-limiting conditions in eukaryotes. Along with its conserved role as a master regulator of sugar starvation responses, SnRK1 is involved in controlling the developmental plasticity and resilience under diverse environmental conditions in plants. In this review, through mining and analyzing the interactome and phosphoproteome data of SnRK1, we are highlighting its role in fundamental cellular processes such as gene regulation, protein synthesis, primary metabolism, protein trafficking, nutrient homeostasis, and autophagy. Along with the well-characterized molecular interaction in SnRK1 signaling, our analysis highlights several unchartered regions of SnRK1 signaling in plants such as its possible communication with chromatin remodelers, histone modifiers, and inositol phosphate signaling. We also discuss potential reciprocal interactions of SnRK1 signaling with other signaling pathways and cellular processes, which could be involved in maintaining flexibility and homeostasis under different environmental conditions. Overall, this review provides a comprehensive overview of the SnRK1 signaling network in plants and suggests many novel directions for future research.
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43

Sales, N. M. R., P. B. Pelegrini, and M. C. Goersch. "Nutrigenomics: Definitions and Advances of This New Science." Journal of Nutrition and Metabolism 2014 (2014): 1–6. http://dx.doi.org/10.1155/2014/202759.

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The search for knowledge regarding healthy/adequate food has increased in the last decades among the world population, researchers, nutritionists, and health professionals. Since ancient times, humans have known that environment and food can interfere with an individual’s health condition, and have used food and plants as medicines. With the advance of science, especially after the conclusion of the Human Genome Project (HGP), scientists started questioning if the interaction between genes and food bioactive compounds could positively or negatively influence an individual’s health. In order to assess this interaction between genes and nutrients, the term “Nutrigenomics” was created. Hence, Nutrigenomics corresponds to the use of biochemistry, physiology, nutrition, genomics, proteomics, metabolomics, transcriptomics, and epigenomics to seek and explain the existing reciprocal interactions between genes and nutrients at a molecular level. The discovery of these interactions (gene-nutrient) will aid the prescription of customized diets according to each individual’s genotype. Thus, it will be possible to mitigate the symptoms of existing diseases or to prevent future illnesses, especially in the area of Nontransmissible Chronic Diseases (NTCDs), which are currently considered an important world public health problem.
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Niu, Tianhua, and Simin Liu. "Gene-Nutrient Interaction in Type 2 Diabetes: An Appraisal of the Role of the Peroxisome Proliferator-Activated Receptor Pathway." Current Pharmacogenomics 3, no. 2 (June 1, 2005): 119–28. http://dx.doi.org/10.2174/1570160054022953.

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Lelandais-Brière, Christine, Jérémy Moreau, Caroline Hartmann, and Martin Crespi. "Noncoding RNAs, Emerging Regulators in Root Endosymbioses." Molecular Plant-Microbe Interactions® 29, no. 3 (March 2016): 170–80. http://dx.doi.org/10.1094/mpmi-10-15-0240-fi.

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Endosymbiosis interactions allow plants to grow in nutrient-deficient soil environments. The arbuscular mycorrhizal (AM) symbiosis is an ancestral interaction between land plants and fungi, whereas nitrogen-fixing symbioses are highly specific for certain plants, notably major crop legumes. The signaling pathways triggered by specific lipochitooligosaccharide molecules involved in these interactions have common components that also overlap with plant root development. These pathways include receptor-like kinases, transcription factors (TFs), and various intermediate signaling effectors, including noncoding (nc)RNAs. These latter molecules have emerged as major regulators of gene expression and small ncRNAs, composed of micro (mi)RNAs and small interfering (si)RNAs, are known to control gene expression at transcriptional (chromatin) or posttranscriptional levels. In this review, we describe exciting recent data connecting variants of conserved si/miRNAs with the regulation of TFs, such as NSP2, NFY-A1, auxin-response factors, and AP2-like proteins, known to be involved in symbiosis. The link between hormonal regulations and these si- and miRNA-TF nodes is proposed in a model in which different feedback loops or regulations controlling endosymbiosis signaling are integrated. The diversity and emerging regulatory networks of young legume miRNAs are also highlighted.
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Bulloch, Rhodi E., Clare R. Wall, Lesley M. E. McCowan, Rennae S. Taylor, Claire T. Roberts, and John M. D. Thompson. "The Effect of Interactions between Folic Acid Supplementation and One Carbon Metabolism Gene Variants on Small-for-Gestational-Age Births in the Screening for Pregnancy Endpoints (SCOPE) Cohort Study." Nutrients 12, no. 6 (June 4, 2020): 1677. http://dx.doi.org/10.3390/nu12061677.

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Small-for-gestational-age (SGA) is associated with significant perinatal morbidity and mortality. Our aim was to investigate gene-nutrient interactions between maternal one-carbon single nucleotide polymorphisms (SNPs) and folic acid supplement (FAS) use, and their association with SGA. Nulliparous New Zealand women with singleton pregnancy were recruited as part of the Screening for Pregnancy Endpoints prospective cohort study. Data on FAS use was collected via face-to-face interview at 15 weeks’ gestation; participants were followed prospectively and birth outcome data collected within 72 h of delivery. Participants were genotyped for MTHFR 677, MTHFR 1298, MTHFD1 1958, MTR 2756, MTRR 66 and TCN2 776 SNPs. Genotype data for at least one SNP was available for 1873 (93%) of eligible participants. Analysis showed a significant SNP-FAS interaction for MTHFR 1298 (p = 0.020), MTHFR 677 (p = 0.019) and TCN2 776 (p = 0.017) in relation to SGA: MTHFR 1298 CC variant non-FAS users had an increased likelihood [Odds Ratio (OR) = 2.91 (95% Confidence Interval (CI) = 1.52, 5.60] compared with wild-type (MTHFR 1298 AA) FAS users. MTHFR 677 variant allele carrier (MTHFR 677 CT + MTHFR 677 TT) non-FAS users had an increased likelihood [OR = 1.87 (95% CI = 1.21, 2.88)] compared to wild-type (MTHFR 677 CC) FAS users. TCN2 776 variant (TCN2 776 GG) non-FAS users had an increased likelihood [OR = 2.16 (95% CI = 1.26, 3.71)] compared with wild type homozygote + heterozygote (TCN2 776 CC + TCN2 776 CG) FAS users. No significant interactions were observed for MTHFD1 1958, MTR 2756 or MTRR 66 (p > 0.05). We observed an overall pattern of FAS attenuating differences in the likelihood of SGA seen between genotype groups in FAS non-users. Future research should focus on how intake of other one-carbon nutrients might mediate these gene-nutrient interactions.
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Nguyen, Minh, Milán Somogyvári, and Csaba Sőti. "Hsp90 Stabilizes SIRT1 Orthologs in Mammalian Cells and C. elegans." International Journal of Molecular Sciences 19, no. 11 (November 20, 2018): 3661. http://dx.doi.org/10.3390/ijms19113661.

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Sirtuin 1 (SIRT1) othologs are ubiquitous NAD+-dependent deacetylases that act as nutrient sensors and modulate metabolism and stress responses in diverse organisms. Both mammalian SIRT1 and Caenorhabditis elegans SIR-2.1 have been implicated in dietary restriction, longevity, and healthspan. Hsp90 is an evolutionarily conserved molecular chaperone that stabilizes a plethora of signaling ’client’ proteins and regulates fundamental biological processes. Here we report that Hsp90 is required for conformational stabilization of SIRT1 and SIR-2.1. We find that inhibition of Hsp90 by geldanamycin (GA) induces the depletion of mammalian SIRT1 protein in a concentration and time dependent manner in COS-7 and HepG2 cells. In contrast to SIRT1, SIRT2 level remains unchanged by GA treatment, reflecting a specific Hsp90 SIRT1 interaction. Hsp90 inhibition leads to the destabilization and proteasomal degradation of SIRT1. Moreover, we observe a GA-sensitive physical interaction between SIRT1 and Hsp90 by immunoprecipitation. We also demonstrate that hsp-90 gene silencing also induces SIR-2.1 protein depletion and proteasomal degradation in C. elegans. Our findings identify metazoan SIRT1 orthologs as Hsp90 clients and reveal a novel crosstalk between the proteostasis and nutrient signaling networks, which may have implications in various age related diseases.
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Requena, Natalia, Petra Füller, and Philipp Franken. "Molecular Characterization of GmFOX2, an Evolutionarily Highly Conserved Gene from the Mycorrhizal Fungus Glomus mosseae, Down-Regulated During Interaction with Rhizobacteria." Molecular Plant-Microbe Interactions® 12, no. 10 (October 1999): 934–42. http://dx.doi.org/10.1094/mpmi.1999.12.10.934.

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Arbuscular mycorrhizal (AM) fungi form the most widespread symbiosis of the plant kingdom. More than 80% of vascular plants are susceptible to colonization by the zygomycetous fungi from the order Glomales, and profit significantly by the nutrient exchange between plant and fungus. However, knowledge of the biology of these fungi still remains elusive because of their obligate biotrophism and, up to now, unculturability. The molecular mechanisms underlying the presymbiotic stages and the cell-to-cell communication between AM fungi and other soil microorganisms are, particularly, unknown. Here, we study these aspects by means of a molecular approach to monitor changes in the gene expression of the fungus Glomus mosseae (BEG12) in response to the rhizobacterium Bacillus subtilis NR1. The bacterium was found to induce specific increases in mycelial growth as well as changes in expression of GmFOX2, a highly conserved gene encoding a multifunctional protein of the peroxisomal β-oxidation. We determined the gene structure and studied its expression in response to rhizobacteria at two time points. The results show that the fungus is able to change its gene expression in response to stimuli other than the plant.
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Rahnama, M., R. D. Johnson, C. R. Voisey, W. R. Simpson, and D. J. Fleetwood. "The Global Regulatory Protein VelA Is Required for Symbiosis Between the Endophytic Fungus Epichloë festucae and Lolium perenne." Molecular Plant-Microbe Interactions® 31, no. 6 (June 2018): 591–604. http://dx.doi.org/10.1094/mpmi-11-17-0286-r.

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Epichloë species fungi form bioprotective endophytic symbioses with many cool-season grasses, including agriculturally important forage grasses. Despite its importance, relatively little is known about the molecular details of the interaction and the regulatory genes involved. The conserved velvet-domain protein VelA (or VeA) is a global regulator of a number of cellular and developmental functions in fungi. In this study, the E. festucae velA gene was functionally characterized in vitro and during interaction with perennial ryegrass. The velA gene is required in E. festucae for resistance to osmotic and cell wall–damaging stresses, repression of conidiation, and normal hyphal morphology during nutrient-limited in-vitro conditions. Expression of velA in E. festucae is light- and nitrogen-dependent and is tissue-specific in mature infected plants. In-planta studies showed that velA is required in E. festucae for a compatible interaction. Inoculating seedlings with mutant ΔvelA induced callose deposition and H2O2 production, and a high level of seedling death was observed. In surviving plants infected with ΔvelA mutant fungi, plants were stunted and we observed increased biomass and invasion of vascular bundles. Overall, this work characterizes a key fungal regulatory factor in this increasingly important model symbiotic association.
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Sultana, Halima, Ayaka Kato, Ai Ohashi, Rie Takashima, Tomoko Katsurai, Shoko Sato, Masafumi Monma, et al. "Effect of Vitamin K-Mediated PXR Activation on Drug-Metabolizing Gene Expression in Human Intestinal Carcinoma LS180 Cell Line." Nutrients 13, no. 5 (May 18, 2021): 1709. http://dx.doi.org/10.3390/nu13051709.

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The pregnane X receptor (PXR) is the key regulator of our defense mechanism against foreign substances such as drugs, dietary nutrients, or environmental pollutants. Because of increased health consciousness, the use of dietary supplements has gradually increased, and most of them can activate PXR. Therefore, an analysis of the interaction between drugs and nutrients is important because altered levels of drug-metabolizing enzymes or transporters can remarkably affect the efficiency of a co-administered drug. In the present study, we analyzed the effect of vitamin K-mediated PXR activation on drug metabolism-related gene expression in intestine-derived LS180 cells via gene expression studies and western blotting analyses. We demonstrated that menaquinone 4 (MK-4), along with other vitamin Ks, including vitamin K1, has the potential to induce MDR1 and CYP3A4 gene expression. We showed that PXR knockdown reversed MK-4-mediated stimulation of these genes, indicating the involvement of PXR in this effect. In addition, we showed that the expression of MDR1 and CYP3A4 genes increased synergistically after 24 h of rifampicin and MK-4 co-treatment. Our study thus elucidates the importance of drug–nutrient interaction mediated via PXR.
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