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Feedstock type influences bacterial and methanogenic communities in anaerobic digestion. These two communities work tightly to maintain the stability of anaerobic digestion. How to quick report the changes of microbial community structure especially methanogenesis is the key issue for optimizing anaerobic digestion process. In this study, 13C isotope fractionations of CH4 and CO2 in biogas and microbial community composition were analyzed in 5 different feedstocks. Our results showed that grass silage, maize silage and swine manure fed reactors had similar δ 13C values and methanogenic community composition, dominated by Methanosarcinaceae. The lowest δ 13CH4 values were detected in straw and chicken manure fed reactors, reflecting reduced microbial degradation of material or the presence of toxic components in these feedstocks. The straw fed bioreactor lead to low δ 13CH4 values, probably reflecting relatively high levels of the syntrophic acetate oxidizing bacteria, Synergistaceae and Syntrophaceae, which might work collectively with hydrogenotrophic methanogens, resulting in the low δ 13CH4 values in this bioreactor. Significantly, all core microbes in the 5 different feedstock fed bioreactors were either Clostridia species or related to the Synergistaceae (syntrophic acetate oxidizing bacteria).

The orchestration of various biological processes with high fidelity requires a precise control over temporal and spatial expression of genes. The regulation of gene expression in eukaryotes can occur at various steps, namely, transcription, m-RNA splicing, translation, and Posttranslational modifications. Transcriptional control can be achieved at any of the various stages—initiation, elongation, and termination. Initiation is marked by the assembly of the preinitiation complex at the promoter of the corresponding gene. However, at the centre of all of this is the basic process of the TF finding the right cis-regulatory motif. This is an extremely important event, as this decides when the polymerase, which is walking or hopping across the DNA molecule stops and starts synthesizing the mRNA molecules. In this article, we shall aim to propose a Rejection model, which may be followed by the basic TFs to find the right promoters for transcription. We hypothesize that the binding of TF occurs in two steps – an initial low-specificity binding event to similar cis-regulatory sequences, which may be strong or weak binding motifs, followed by a process of scrutiny and rejection of weaker binding sequences.

NLRP3 is associated with multiple risks in graft-versus-host disease, though unifying principles for these findings remain largely unknown. To explore the effects and mechanisms of the absence of NLRP3 function on hepatic graft-versus-host-disease, we established an allogeneic hematopoietic cell transplantation mice model by infusing bone marrow mononuclear cells and spleno-T cells of the BALB/c mouse into either NLRP3 knockout (NLRP3-/- ) or wild-type C57BL/6 mice. Elevated inflammatory cell infiltration, liver fibrosis, and secretions of alanine aminotransferase (ALT) and aspartate transaminase (AST), together with weight loss, were observed in C57BL/6 recipients after transplantation. However, moderate injury pathology was detected in the liver of NLRP3-/- recipients at day 14, which gradually improved over time. Likewise, proinflammatory cytokine IL-1β, a downstream effecter of NLRP3 inflammasome activation, showed significantly lower expression (P < .05) in the liver of NLRP3-/- recipients relative to C57BL/6 recipients at day 7 and day 21. Moreover, compared with C57BL/6 recipients, the expression of both TNF-α and IL-1β were decreased 3-fold and 4.7-fold, respectively, at day 21 in NLRP3-/- recipients. Interestingly, NLRP1a was expressed at a significantly reduced level in the liver of NLRP3-/- recipients (P < .001). Furthermore, systemic inflammation was analyzed by measuring the concentration of IL-1β and adenosine triphosphate (ATP) in serum. The concentration of IL-1β achieved a maximum at day 14, then decreased at day 21 and day 28 in NLRP3-/- recipients. In contrast, the concentration of IL-1β in C57BL/6 recipients gradually increased from day 7 to day 28. ATP levels reduced from day 7 to day 28 in NLRP3-/- recipients, but were extremely high in C57BL/6 recipients from day 14 to day 28 (P < .01). The decreased levels of P2X7R were connected to less ATP in NLRP3-/- recipients at day 21 and day 28. In conclusion, NLRP3 knockout in recipients could significantly relieve liver injury after transplantation and block the NLRP3 inflammasome pathway, thus providing a promising strategy for the treatment of graft-versus-host disease prophylaxis.

De-etiolation is indispensable for seedling survival and development. However, how sugars regulate de-etiolation and how sugars induce ethylene (ET) for seedlings to grow out of soil remain elusive. Here, we reveal how a sucrose (Suc) feedback loop promotes de-etiolation by inducing ET biosynthesis. Under darkness, Suc in germinating seeds preferentially induces 1-amino-cyclopropane-1-carboxylate synthase (ACS7; encoding a key ET biosynthesis enzyme) and associated ET biosynthesis, thereby activating ET core component ETHYLENE-INSENSITIVE3 (EIN3). Activated EIN3 directly inhibits the function of Suc transporter 2 (SUC2; a major Suc transporter) to block Suc export from cotyledons and thereby elevate Suc accumulation of cotyledons to induce ET. Under light, ET-activated EIN3 directly inhibits the function of phytochrome A (phyA; a de-etiolation inhibitor) to promote de-etiolation. We therefore propose that under darkness, the Suc feedback loop (Suc-ACS7-EIN3-|SUC2-Suc) promotes Suc accumulation in cotyledons to guarantee ET biosynthesis, facilitate de-etiolation, and enable seedlings to grow out of soil.

A key feature following pathogen recognition by resistance (R) proteins containing NB-ARC (nucleotide-binding adaptor shared by Apaf-1, R proteins, and Ced-4) domains is the hypersensitive response (HR). However, the underpinning mechanisms integral to this process remain relatively opaque. Here we show that a gain-of-function mutation in the NB-ARC protein, RLS1 (Rapid Leaf Senescence1), triggers high-light-dependent HR-like cell death in rice. The RLS1-mediated defense response is independent of SA (salicylic acid) accumulation, NPR1 (nonexpressor of pathogenesis-elated genes 1) activity and RAR1 (required for Mla12 resistance1) function. A screen for suppressors of RLS1 activation identified RMC (Root Meander Curling), a cysteine-rich receptor-like secreted protein (CRRSP). RMC is essential for the RLS1 activated defense response via functioning as a RLS1-binding partner and subsequently suppressing the activity of key antioxidant enzymes. Collectively, our findings reveal a NB-ARC-CRRSP signaling module that triggers HR-like cell death and associated disease resistance in rice.

Ethnopharmacological relevance: Traditional knowledge is a particular form of practice or skill set that was developed in ancient times and was sustained through generations via the passing of knowledge, essentially confined within a specific tribe, local people, or family lineages. Ethnodermatological use of medicinal plants in India is still a subject to conduct more studies to see if there is chemical, microbiological, and/or clinical evidence, from a scientific perspective, of their effectiveness for those skin disorders. Thus, this review can be the basis for further studies and may provide targets for drug development. Aim of the study: We compile and emphasize the most important part of ethnodermatology, namely, traditional knowledge of medicinal plants and their applications for several skin diseases in India. We also include a brief review and explanation on dermatology in Ayurvedic and Unani medicine. We review the pharmacological activity of extracts derived from some of the most cited plants against problem skin diseases as well. Materials and methods: Different kinds of key phrases such as “Indian traditional ethnodermatology”, “ethnodermatology”, “ethnobotany”, “skin diseases”, “Ayurveda dermatology”, “pharmacological activity” were searched in online search servers/databases such as Google Scholar (https://scholar.google.com/), ResearchGate (https://www.researchgate.net/), PubMed (https://pubmed.ncbi.nlm.nih.gov/), NISCAIR Online Periodicals Repository (NOPR) (http://nopr.niscair.res.in/). Based upon the analyses of data obtained from 178 articles, we formulated several important findings which are a summary shown in Tables. Tables. A total of 119 records of plants’ uses have been found across India against 39 skin diseases. These are depicted with their localities of report, parts used, and preparation and administration methods against particular skin diseases. Results: The knowledge and utilisation of herbal medicine in the Indian subcontinent has great potential to treat different kinds of human skin disorders. The administration of extracts from most of the plant species used is topical and few only are administrated orally. We also investigated the pharmacological activity of the extracts of the most cited plants against mice, bacterial and fungal pathogens, and human cells. Conclusions: Complementary therapy for dermatological problems and treatment remains the main option for millions of people in the Indian subcontinent. This review on the practices of ethnobotanical dermatology in India confirms the belief that their analysis will accelerate the discovery of new, effective therapeutic agents for skin diseases. However, more studies and clinical evidence are still required to determine if the identified species may contribute to skin condition treatment, particularly in atopic eczema. Today, ethnodermatology is a well-accepted international discipline and many new practices have been initiated in numerous countries. We hope this article will further accelerate the development of this area to identify a new generation of natural human skin treatments that will help meet the growing consumer demand for safe, sustainable, and natural treatments. In this context, research on plants utilised in ethnodermatology in India and elsewhere should be intensified.

With the threat of certain plant protection products becoming ineffective due to reduced pathogen sensitivity to fungicides or through the removal of products due to changes in legislation, alternative compounds are sought for use in disease management programmes. The effects of an arabinoxylan film-forming polymer derived from maize cell walls to control crop diseases of spring barley was assessed in field experiments. Control of powdery mildew, Rhynchosporium scald, and Ramularia leaf spot on barley was achieved with the polymer but control was inconsistent between trials. However, good levels of disease control were observed when the polymer was applied with a reduced fungicide programme. No yield penalties were associated with use of the polymer in any trial irrespective of the level of disease control. Alternative plant protection products such as this arabinoxylan polymer may be useful components in future integrated disease management strategies aimed at reducing fungicide inputs without any cost to disease control.

The production of the redox-active signaling molecule, NO, has long been associated with interactions between microbes and their host plants. Emerging evidence now suggests that specific NO signatures and cognate patterns of PHYTOGLOBIN1 (PHYTOGB1) expression, a key regulator of cellular NO homeostasis, may help determine either symbiosis or pathogenicity.

Plant cell culture constitutes a sustainable, controllable and environmentally friendly tool to produce natural products for the pharmaceutical, cosmetic and industrial biotechnology industries. However, there are significant obstacles to the commercial synthesis of high value chemicals from plant culture including low yields, performance instability, slow plant cell growth, industrial scale-up and downstream processing. Cambial meristematic cells constitute a platform to ameliorate many of these potential problems enabling the commercial production of high value chemicals.

In eukaryotes, bursts of reactive oxygen and nitrogen species mediate cellular responses to the environment by modifying cysteines of signaling proteins. Cysteine reactivity toward nitric oxide (NO) leads to formation of S-nitrosothiols (SNOs) that play important roles in pathogenesis and immunity. However, it remains poorly understood how SNOs are employed as specific, reversible signaling cues. Here we show that in plant immunity the oxidoreductase Thioredoxin-h5 (TRXh5) reverses SNO modifications by acting as a selective protein-SNO reductase. While TRXh5 failed to restore immunity in gsnor1 mutants that display excessive accumulation of the NO donor S-nitrosoglutathione, it rescued immunity in nox1 mutants that exhibit elevated levels of free NO. Rescue by TRXh5 was conferred through selective denitrosylation of excessive protein-SNO, which reinstated signaling by the immune hormone salicylic acid. Our data indicate that TRXh5 discriminates between protein-SNO substrates to provide previously unrecognized specificity and reversibility to protein-SNO signaling in plant immunity.

Plants are capable of producing a wide variety of secondary metabolites which have a diverse range of functions that can be exploited for medicinal purposes; for example, paclitaxel is a major anti-cancer drug found in the bark of Taxus spp. There are however supply issues as the compound is only found at low concentrations (0.05%) within the plant. The complex paclitaxel biosynthetic pathway makes chemical synthesis non-commercially viable; therefore alternative biotechnological sources have been explored for production including heterologous expression systems and plant cell culture.

Background Reactive oxygen and nitrogen intermediates (ROIs and RNIs), respectively, are central features of the plant immune response. Rare, highly reactive protein cysteine (Cys) residues of low pKa are a major target for these intermediates. In this context, S-nitrosylation, the addition of a nitric oxide (NO) moiety to a Cys thiol to form an S-nitrosothiol (SNO), is emerging as a key, redox-based post-translational modification during plant immune function. Methods Here, we describe some recent insights into how ROIs and RNIs are synthesized and how these small, redox active molecules help orchestrate the plant defence response. Results The reviewed data highlights the growing importance of ROIs and RNIs in orchestrating the development of plant immunity and provides insights into the molecular mechanisms underpinning their function. General significance Signalling via small, redox active molecules is a key feature underpinning a diverse series of signal transduction networks in eukaryotic cells. Therefore, insights into the mechanisms that support the activity of these molecules may have potentially wide significance. This article is part of a Special Issue entitled: Regulation of cellular processes by S-nitrosylation.

Changes in cellular redox status are a conspicuous feature of immune responses in a variety of eukaryotes, but the associated signaling mechanisms are not well understood. In plants, attempted microbial infection triggers the rapid synthesis of nitric oxide (NO) and a parallel accumulation of reactive oxygen intermediates (ROIs). The emerging data suggests these small, redox-active molecules orchestrate a plethora of immune responses. In this context, we are principally exploring S-nitrosylation, the addition of an NO moiety to a rare, highly reactive protein cysteine thiol to form an S-nitrosothiol (SNO). This key redox-based, post-translational modification is becoming established as a central mechanism to regulate plant immune responses, including: control of ROI synthesis, accumulation of the immune activator, salicylic acid, pathogen-triggered, hypersensitive cell death and also defense strategies at the plant cell wall. I will present some of our recent work associated with this research area.

Cell death is an important aspect of plant resistance to pathogen infection. Recent results have shed new light on the mechanisms that control this cell death following attempted pathogen infection.

Expression of the French bean chalcone synthase ( CHS ) gene is induced in response to external stimuli and to the plant's tissue-specific and developmental program. We have previously demonstrated the essential role of a cooperative regulatory element (CAR), containing a G-box and H-box, in tissue-specific expression. In this paper, we focus on understanding the requirement for cis -elements in the response of the CHS15 promoter to the abiotic elicitor HgCl 2 , mechanical wounding and infection with tobacco mosaic virus (TMV). Leaves of tobacco plants transformed with a chimeric CHS15 promoter-β-glucuronidase gene construct carrying a mutation at the G-box did not exhibit impaired promoter response to wounding, but did show a 19% reduction in the response to HgCl 2 and TMV. A mutation at the H-box within CAR resulted in a 30% increase in promoter response to wounding and reductions of 36 and 54% in the response to HgCl 2 and TMV, respectively. These results suggest differential utilization of regulatory cis -elements for stress-induced and tissue-specific expression of the bean CHS15 promoter.

Candida albicans is a major fungal pathogen that causes frequent mucosal infections in otherwise healthy individuals, and life-threatening systemic infections in immune-compromised patients. The first line of defence against Candida albicans is the release of reactive nitrogen species (RNS), reactive oxygen species (ROS) and cationic fluxes by macrophages and neutrophils. As a result robust responses to RNS, ROS and cationic stresses play major roles in the virulence of C. albicans . This fungus is exposed to all of these stresses simultaneously following phagocytosis. Consequently in this study we examined the responses of this pathogen to combinations of nitrosative, oxidative and cationic stress. The roles of the Cta4-Yhb1, Cap1, Hog1 and Mkc1 signalling pathways, which activate responses to individual nitrosative, oxidative, cationic and cell wall stresses, respectively, were examined. The sensitivity of null mutants to individual and combinatorial stresses was examined, and the activation of these pathways was confirmed by assaying the phosphorylation levels of the key protein kinases. Further evidence of the pathway activation was provided by transcription factor localisation and the expression of downstream target genes. We show that combinatorial nitrosative, oxidative and/or cationic stresses exert unexpected effects upon the classical stress signalling pathways. The relevance to C. albicans infections will be discussed.