Common bean (Phaseolus vulgaris L.) is one of the most important grain legumes worldwide. Polyphenols are the predominant bioactive components with multifold bioactivities in diverse common bean cultivars. Phenolic acids, flavonoids, and proanthocyanidins are the main polyphenols in common beans, and colorful common beans are overall rich in polyphenols, mainly in their pigmented seed coats. In addition, factors of influence, such as genotype, environmental conditions, storage, and processing methods, play a critical role in the content and composition of common bean polyphenols. Besides, analytical methods, including extraction, separation, and identification, are of importance for precise and comparable evaluation of polyphenols in common beans. Therefore, in order to provide a comprehensive and updated understanding of polyphenols in common beans, this review first summarizes the content and different compositions of polyphenols in common beans, and next discusses the factors affecting these compositions, followed by introducing the analytical methods for common bean polyphenols, and finally highlights the antioxidant activity of polyphenols in common beans. Considering the recent surge in interest in the use of grain legumes, we hope this review will further stimulate work in this field by providing a blueprint for further analytical studies to better utilize common bean polyphenols in food products to improve human nutrition.
Xanthomonas campestris pv. campestris is the pathogen of black rot of cruciferous plants. The pathogenicity of the pathogen depends on the type III secretion system (T3SS) that translocates directly effector proteins into plant cells, where they play important roles in the molecular interaction between the pathogen and its hosts. The T3SS of Xanthomonas spp. is encoded by a cluster of hypersensitive response and pathogenicity (hrp) genes. It has been demonstrated that the expression of hrp genes and some type III secreted (T3S)-effector genes is coactivated by the key hrp regulatory protein HrpX. The regulation by HrpX can be mediated by the binding of HrpX protein to a cis-regulatory element named the plant-inducible promoter (PIP) box present in the promoter region of HrpX-regulated genes. A genome screen revealed that X. campestris pv. campestris 8004 possesses 56 predicted genes with the PIP box. Nine of these genes have been shown to encode T3S effectors, Hrp, and Hrp-associated proteins. In this study, we employed an established T3S effector translocation assay with the hypersensitive-reaction-inducing domain of X. campestris pv. campestris AvrBs1 as a reporter to characterize the remaining 47 genes with the PIP box and showed that 6 of them, designated as XopXccE1, XopXccP, XopXccQ, XopXccR1, XopXccLR, and AvrXccB, harbor a functional translocation signal in their N-terminal regions, indicating that they are T3S effectors of X. campestris pv. campestris. We provided evidence to demonstrate that all these effectors are expressed in an HrpX-dependent manner and their translocation into plant cells relies on the translocon protein HrpF and the chaperone HpaB. Mutational analyses demonstrated that all these effectors, except AvrXccB, are individually required for full virulence and growth of X. campestris pv. campestris in the host plant Chinese radish.
Reticulon 3 (RTN3) has previously been shown to interact with BACE1 and negatively regulate BACE1 activity. To what extent RTN3 deficiency affects BACE1 activity is an intriguing question. In this study, we aimed to address this by generating RTN3-null mice. Mice with complete deficiency of RTN3 grow normally and have no obviously discernible phenotypes. Morphological analyses of RTN3-null mice showed no significant alterations in cellular structure, although RTN3 is recognized as a protein contributing to the shaping of tubular endoplasmic reticulum. Biochemical analysis revealed that RTN3 deficiency increased protein levels of BACE1. This elevation of BACE1 levels correlated with enhanced processing of amyloid precursor protein at the -secretase site. We also demonstrated that RTN3 deficiency in Alzheimer's mouse models facilitates amyloid deposition, further supporting an in vivo role of RTN3 in the regulation of BACE1 activity. Since it has been shown that RTN3 monomer is reduced in brains of Alzheimer's patients, our results suggest that long-lasting reduction of RTN3 levels has adverse effects on BACE1 activity and may contribute to Alzheimer's pathogenesis.
Pathogenic bacteria utilize type 3 secretion systems to inject type 3 effectors (T3Es) into host cells, thereby subverting host defense reactions. Similarly, T3Es of symbiotic nitrogen-fixing rhizobia can affect nodule formation on roots of legumes. Previous work showed that NopL (nodulation outer protein L) of Sinorhizobium(Ensifer) sp. strain NGR234 is multiply phosphorylated in eukaryotic cells and that this T3E suppresses responses mediated by mitogen-activated protein (MAP) kinase signaling in yeast (mating pheromone signaling) and plant cells (expression of pathogenesis-related defense proteins). Here, we show that NopL is a MAP kinase substrate. Microscopic observations of fluorescent fusion proteins and bimolecular fluorescence complementation analysis in onion cells indicated that NopL is targeted to the nucleus and forms a complex with SIPK (salicylic acid-induced protein kinase), a MAP kinase of tobacco. In vitro experiments demonstrated that NopL is phosphorylatyed by SIPK. At least nine distinct spots were observed after two-dimensional gel electrophoresis, indicating that NopL can be hyperphosphorylated by MAP kinases. Senescence symptoms in nodules of beans (Phaseolus vulgaris cv. Tendergreen) were analyzed to determine the symbiotic effector activity of different NopL variants with serine to alanine substitutions at identified and predicted phosphorylation sites (serine-proline motif). NopL variants with six or eight serine to alanine substitutions were partially active, whereas NopL forms with 10 or 12 substituted serine residues were inactive. In conclusion, our findings provide evidence that NopL interacts with MAP kinases and reveals the importance of serine-proline motifs for effector activity during symbiosis.
Pathological features in Alzheimer’s brains include mitochondrial dysfunction and dystrophic neurites (DNs) in areas surrounding amyloid plaques. Using a mouse model that overexpresses reticulon 3 (RTN3) and spontaneously develops age-dependent hippocampal DNs, here we report that DNs contain both RTN3 and REEPs, topologically similar proteins that can shape tubular endoplasmic reticulum (ER). Importantly, ultrastructural examinations of such DNs revealed gradual accumulation of tubular ER in axonal termini, and such abnormal tubular ER inclusion is found in areas surrounding amyloid plaques in biopsy samples from AD brains. Functionally, abnormally clustered tubular ER induces enhanced mitochondrial fission in the early stages of DN formation and eventual mitochondrial degeneration at later stages. Furthermore, such DNs are abrogated when RTN3 is ablated in aging and AD mouse models. Hence, abnormally clustered tubular ER can be pathogenic in brain regions: disrupting mitochondrial integrity, inducing DNs formation and impairing cognitive function in AD and aging brains
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