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Anthocyanins are natural water-soluble pigments that are important in plants because they endow a variety of colors to vegetative tissues and reproductive plant organs, mainly ranging from red to purple and blue. The colors regulated by anthocyanins give plants different visual effects through different biosynthetic pathways that provide pigmentation for flowers, fruits and seeds to attract pollinators and seed dispersers. The biosynthesis of anthocyanins is genetically determined by structural and regulatory genes. MYB (v-myb avian myeloblastosis viral oncogene homolog) proteins are important transcriptional regulators that play important roles in the regulation of plant secondary metabolism. MYB transcription factors (TFs) occupy a dominant position in the regulatory network of anthocyanin biosynthesis. The TF conserved binding motifs can be combined with other TFs to regulate the enrichment and sedimentation of anthocyanins. In this study, the regulation of anthocyanin biosynthetic mechanisms of MYB-TFs are discussed. The role of the environment in the control of the anthocyanin biosynthesis network is summarized, the complex formation of anthocyanins and the mechanism of environment-induced anthocyanin synthesis are analyzed. Some prospects for MYB-TF to modulate the comprehensive regulation of anthocyanins are put forward, to provide a more relevant basis for further research in this field, and to guide the directed genetic modification of anthocyanins for the improvement of crops for food quality, nutrition and human health.

Plant root system plasticity is critical for survival in changing environmental conditions. One important aspect of root architecture is lateral root development, a complex process regulated by hormone, environmental and protein signalling pathways. Here we show, using molecular genetic approaches, that the MYB transcription factor AtMYB93 is a novel negative regulator of lateral root development in Arabidopsis. We identify AtMYB93 as an interaction partner of the lateral‐root‐promoting ARABIDILLO proteins. Atmyb93 mutants have faster lateral root developmental progression and enhanced lateral root densities, while AtMYB93‐overexpressing lines display the opposite phenotype. AtMYB93 is expressed strongly, specifically and transiently in the endodermal cells overlying early lateral root primordia and is additionally induced by auxin in the basal meristem of the primary root. Furthermore, Atmyb93 mutant lateral root development is insensitive to auxin, indicating that AtMYB93 is required for normal auxin responses during lateral root development. We propose that AtMYB93 is part of a novel auxin‐induced negative feedback loop stimulated in a select few endodermal cells early during lateral root development, ensuring that lateral roots only develop when absolutely required. Putative AtMYB93 homologues are detected throughout flowering plants and represent promising targets for manipulating root systems in diverse crop species.

In order to investigate the relationship between dissolved silicon (DSi) and bicarbonate (HCO3–), we analysed water samples from the main Changjiang channel and its main tributaries in August 2006 and, during 2007-2009, the contrasting tributaries Wujiang (WJ) – mainly dominated by carbonate weathering, and Ganjiang – mainly dominated by silicate weathering. The DSi: HCO3– ratio ranged from 0 to 0.67, which is in agreement with mixing between the weathering of carbonate or silicate. A negative correlation between DSi and HCO3– was observed and interpreted as the imprint of regional geology on water chemistry. This relationship and the DSi: HCO3– ratios illustrate the predominant role of carbonate weathering on the riverine HCO3–, even forcatchments where silicate rocks are dominant. In contrast, a cascade of dams in WJ tributary influenced the concentrations of Dsi and HCO3– and resulted in a positive correlation between DSi and HCO3–. This is because reservoirs allowed populations of diatomsto develop and diatoms stoichiometrically sequestered DSi and HCO3– causing a negative feedback regulation on the DSi: HCO3– ratio. Our study demonstrates that the relationship between DSi and HCO3–can reflect not only their geological background but also the influence of algal activity (diatom uptake) within rivers.

Interleukin-1 (IL-1) is a primary cytokine of innate immunity and inflammation. IL-1 belongs to a complex family including ligands with agonist activity, receptor antagonists, and an anti-inflammatory cytokine. The receptors for these ligands, the IL-1 Receptor (IL-1R) family, include signaling receptor complexes, decoy receptors, and negative regulators. Agonists and regulatory molecules co-evolved, suggesting the evolutionary relevance of a tight control of inflammatory responses, which ensures a balance between amplification of innate immunity and uncontrolled inflammation. IL-1 family members interact with innate immunity cells promoting innate immunity, as well as with innate and adaptive lymphoid cells, contributing to their differentiation and functional polarization and plasticity. Here we will review the properties of two key regulatory receptors of the IL-1 system, IL-1R2, the first decoy receptor identified, and IL-1R8, a pleiotropic regulator of different IL-1 family members and co-receptor for IL-37, the anti-inflammatory member of the IL-1 family. Their complex impact in pathology, ranging from infections and inflammatory responses, to cancer and neurologic disorders, as well as clinical implications and potential therapeutic exploitation will be presented.

This article is a Commentary on Tissot et al., 223: 1433–1446

Production of thyroid hormone is precisely regulated in a negative feed-back mechanism that depends critically on thyroid hormone receptor β (TRβ). This mechanism decreases production of thyrotropin- releasing hormone (TRH) and thyrotropin (TSH) in the hypothalamus and pituitary gland in response to high levels of circulating thyroid hormones (TH). Despite the wealth of accumulated knowledge, it is still not clear how exactly this negative regulation is executed. The syndrome of resistance to thyroid hormone (RTH), in which the levels of TH are not properly sensed, represents naturally occurring situations in which molecular components of this regulation are displayed and may be uncovered. TRβ, which is central to this regulation, is in the majority of RTH cases mutated in a way that preserves some functions of the receptor. Approximately 150 different mutations in TRβ have been identified to date. Here, we hypothesized that additional pathogenic mutations in TRβ are likely to exist in human population and analysed clinical cases with suspected RTH. In keeping with our prediction, analysis of 17 patients from nine families led to identification of four presumed pathogenic mutations of TRβ, including a previously unknown mutation, T273R. This suggests that threonine 273 is likely to be critical for the normal function of TRβ, possibly due to its role in helix 12 mobility and interaction with coactivators, and thus supports the concept that TRβ-dependent trans-activating function is necessary for the inhibition of TRH and TSH expression in response to elevated levels of TH.

Key message Overexpression of CpbHLH1 in Arabidopsis and tobacco resulted in a dramatic decrease in anthocyanin accumulation by repressing the expression of late biosynthesis genes in the flavonoid biosynthesis pathway. Many basic helix–loop–helix (bHLH) transcription factors (TFs) of subgroup IIIf have been characterized as anthocyanin-associated activators in higher plants, but information regarding bHLH TFs that inhibit anthocyanin accumulation remains scarce. In this study, the subgroup IIIf bHLH TF CpbHLH1 from Chimonanthus praecox (L.) was identified as a negative regulator of anthocyanin accumulation. Our results showed that overexpression of CpbHLH1 in model plant species, Arabidopsis and tobacco, resulted in a dramatic decrease in anthocyanin content, whereas the content of proanthocyanidin was little affected. Quantitative RT-PCR (qRT-PCR) assays of the structural genes in the flavonoid biosynthesis pathway revealed that CpbHLH1 inhibits anthocyanin accumulation mainly through repressing the expression of late biosynthesis genes (LBGs). Interactions between CpbHLH1 protein and AtPAP1/NtAN2 protein were detected via yeast two-hybrid (Y2H) and bimolecular fluorescence complementation (BiFC) assays. This is the first bHLH repressor of anthocyanin biosynthesis identified in dicotyledons. These results can help us better understand the anthocyanin regulatory network in plants and may provide insights into the diverse functions of bHLH proteins.

The copious and uncontrolled practice of exercise can generate psychological dependence and mood changes. Emotional regulation and negative affectivity are relevant processes for the development of addictive patterns. This study analysed the differences in negative affectivity and emotional regulation based on the practice profile of exercise; the relationship between exercise dependence, emotional regulation, and negative affectivity; and the mediating role of emotional regulation in such relationship. 375 endurance sports practitioners participated. The differences in the physical exercise practice profiles were significant in all the study variables. Exercise dependence correlated positively and significantly with emotional regulation difficulties and with negative affectivity. Emotional regulation difficulties were predictors of exercise dependence. There was a mediating effect of emotional regulation difficulties between negative affect and exercise dependence. Improving emotional regulation skills could prevent the onset of exercise dependence.

The surface Toll-like receptor 9 (sTLR9) has been identified on the surface of the B cells and was presumed to be a negative regulator of B cell responses. CpG ODN, a TLR9 agonist, has been successfully used as an adjuvant of hepatitis B vaccine to enhance antibody responses. However, it is unknown whether the sTLR9 is involved in regulating the activation and maturation of B cells in the antibody responses induced by CpG ODN–adjuvanted vaccines. In this study, we immunized mice with hepatitis B vaccine adjuvanted by CpG ODN (CpG 5805) and found that CpG 5805 enhanced the antibody response to vaccine and meanwhile down-regulated the sTLR9 levels on B cells. With antibody feeding assay and flow cytometry analysis, we further found that CpG 5805 induced a movement of the sTLR9 in B cells, internalized first and then mobilized to endosomes. Accompanied with the movement, CD80, CD86, CD40, and MHC II molecules were significantly up-regulated on the B cells. Interestingly, the B cells with internalized sTLR9 enlarged morphologically, and the sTLR9 levels were obviously lower and CD40 levels were obviously higher on the enlarged B cells. Together, the data presented here uncover that CpG ODN can induce the mobilization and relocation of sTLR9 in B cells, thereby triggering the B cell vigor by relieving the negative regulatory effect of sTLR9 on B cells, which may be one of the mechanisms for CpG ODN acting as a vaccine adjuvant to enhance the antibody response.Key points• CpG ODN–enhanced antibody response positively associates with B cell sTLR9 reduction.• CpG ODN reduces the sTLR9 levels by relocating it from B cell surface to endosomes.• sTLR9 reduction arouses B cell vigor via promoting B cell maturation and activation.

Pathogen infection can cause the production of inflammatory cytokines, which are key mediators that cause the host’s innate immune response. Therefore, proper regulation of immune genes associated with inflammation is essential for immune response. Among them, microRNAs (miRNAs) as gene regulator have been widely reported to be involved in the innate immune response of mammals. However, the regulatory network in which miRNAs are involved in the development of inflammation is largely unknown in lower vertebrates. Here, we identified two miRNAs from miiuy croaker ( Miichthys miiuy ), miR-210 and miR-3570, which play a negative regulatory role in host antibacterial immunity. We found that the expressions of miR-210 and miR-3570 were significantly upregulated under the stimulation of Gram-negative bacterium vibrio harveyi and LPS (lipopolysaccharide). Induced miR-210 and miR-3570 inhibit inflammatory cytokine production by targeting RIPK2, thereby avoiding excessive inflammation. In particular, we found that miR-210 and miR-3570 negatively regulate antimicrobial immunity by regulating the RIPK2-mediated NF-κB signaling pathway. The collective results indicated that both miRNAs are used as negative feedback regulators to regulate RIPK2-mediated NF-κB signaling pathway and thus play a regulatory role in bacteria-induced inflammatory response.