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Abiotic stress is a major factor affecting crop productivity. Chemical priming is a promising strategy to enhance tolerance to abiotic stress. In this study, we evaluated the use of 1-butanol as an effectual strategy to enhance drought stress tolerance in Arabidopsis thaliana. We first demonstrated that, among isopropanol, methanol, 1-butanol, and 2-butanol, pretreatment with 1-butanol was the most effective for enhancing drought tolerance. We tested the plants with a range of 1-butanol concentrations (0, 10, 20, 30, 40, and 50 mM) and further determined that 20 mM was the optimal concentration of 1-butanol that enhanced drought tolerance without compromising plant growth. Physiological tests showed that the enhancement of drought tolerance by 1-butanol pretreatment was associated with its stimulation of stomatal closure and improvement of leaf water retention. RNA-sequencing analysis revealed the differentially expressed genes (DEGs) between water- and 1-butanol-pretreated plants. The DEGs included genes involved in oxidative stress response processes. The DEGs identified here partially overlapped with those of ethanol-treated plants. Taken together, the results show that 1-butanol is a novel chemical priming agent that effectively enhances drought stress tolerance in Arabidopsis plants, and provide insights into the molecular mechanisms of alcohol-mediated abiotic stress tolerance.Key message1-Butanol priming enhances drought tolerance via mechanisms that include stimulating stomatal closure and delaying leaf water loss in Arabidopsis thaliana

The unique fuel characteristics of butanol and the possibility of its microbial production make it one of the most desirable environmentally friendly substitutes for petroleum fuels. However, the highly toxic nature of 1-butanol to the bacterial strains makes it unprofitable for commercial production. By comparison, 2-butanol has similar fuel qualities, and despite the difficulties in its microbial synthesis, it holds promise because it may be less toxic. This paper is the first comprehensive study to compare bacterial tolerance to different butanol isomers by examining the growth of 31 bacterial strains under 1-butanol and 2-butanol stress conditions. The presented results reveal that all tested strains showed a higher tolerance to 2-butanol than to 1-butanol at each solvent concentration (1%, 2%, and 3% v/v). Moreover, with an increased solvent concentration, bacterial cells lost their resistance to 1-butanol more rapidly than to 2-butanol. A comparison of the transcriptome profiles of the reference strains Bacillus subtilis ATCC 168 and E. coli ATCC 25922 disclosed a specific response to butanol stress. Most notably, in the presence of 2-butanol E. coli ATCC 25922 showed a reduced expression of genes for chaperones, efflux pumps, and the flagellar apparatus, as well as an enhancement of membrane and electron transport. B. subtilis, with 2-butanol, did not perform emergency sporulation or escape, as some global transcriptional stress response regulators were downregulated. The overexpression of ribosomal RNAs, pyrimidine biosynthesis genes, and DNA- and RNA-binding proteins such as pcrA and tnpB was crucial in the response.

Wild medicinal herbs have been used as folk and traditional medicines all across the world since well before recorded history. This present study was designed to test the antimicrobial activities of five different solvent extracted samples ( n-hexane , n-butanol , ethyl acetate , methanol , and water ) of Peganum harmala using stems and seeds. Two different strains of Gram-negative bacteria ( Escherichia coli and Klebsiella pneumonia) , two Gram-positive bacteria (Bacillus subtilus and Staphylococcus aureus) , and one fungal strain ( Candida albicans ) were used. The antimicrobial activities were measured using a disc diffusion assay. Two concentrations of the extracts (1 and 2mgDisc -1 ) were used. Ethyl acetate fraction was found more affective among the tested solvents and showed maximum activity (zone of inhibition) against S . aureus ( 65.53 and 81.10% ) , E . coli ( 46.22 and 61.29% ) while n-butanol and water fractions gave maximum activity against S . aureus (78.86 and 70.00%) and K . pneumonia (57.00 and 61.39%) respectively. Water fraction showed maximum activity against C . albicans (60.00 and 81.88%). In the case of the stem, Ethyl acetate again showed more activity against B . subtilus (38.57 and 42.10%) and S. aureus (36.66 and 46.66%) while n-butanol showed maximum activity against K . pneumonia (24.55 and 32.44%) and E . coli (27.93 and 37.61%). Methanol was found more effective against C . albicans (25.71 and 43.80%). Seed extracted samples were found more effective compared to the stem. Ethyl acetate , butanol , and aqueous extracted samples showed good activity against the tested microbes, so these fractions are recommended for study their mechanism of actions and isolation of bioactive metabolites responsible for antimicrobial activities. The P . harmala should be evaluated for their bioactive compounds to be used in future studies. Our objective is to provide the framework for future study on the roles of P . harmala as traditional medicines.

During chemotaxis, activation of the small guanosine triphosphatase Rac is spatially regulated to organize the extension of membrane protrusions in the direction of migration. In neutrophils, Rac activation is primarily mediated by DOCK2, an atypical guanine nucleotide exchange factor. Upon stimulation, we found that DOCK2 rapidly translocated to the plasma membrane in a phosphatidylinositol 3,4,5-trisphosphate-dependent manner. However, subsequent accumulation of DOCK2 at the leading edge required phospholipase D-mediated synthesis of phosphatidic acid, which stabilized DOCK2 there by means of interaction with a polybasic amino acid cluster, resulting in increased local actin polymerization. When this interaction was blocked, neutrophils failed to form leading edges properly and exhibited defects in chemotaxis. Thus, intracellular DOCK2 dynamics are sequentially regulated by distinct phospholipids to localize Rac activation during neutrophil chemotaxis.

To reveal the mechanism of anti-renal fibrosis effects of an -butanol extract from renal fibrosis was induced with unilateral ureteral obstruction (UUO) and then treated with an -butanol extract (BUT) from (Rosaceae). Sixty male Sprague-Dawley rats were randomly divided into the sham-operated, renal fibrosis (RF) model, benazepril hydrochloride-treated model (1.5 mg kg ) and BUT-treated (1.75, 1.5 and 1.25 g kg ) groups and the respective drugs were administered intragastrically for 21 days. Related biochemical indices in rat serum were determined and histopathological morphology observed. Serum metabolomics was assessed with HPLC-Q-TOF-MS. The BUT reduced levels of blood urea nitrogen, serum creatinine and albumin and lowered the content of malondialdehyde and hydroxyproline in tissues. The activity of superoxide dismutase in tissues was increased and an improvement in the severity of RF was observed. Sixteen possible biomarkers were identified by metabolomic analysis and six key metabolic pathways, including the TCA cycle and tyrosine metabolism, were analyzed. After treatment with the extract, 8, 12 and 9 possible biomarkers could be detected in the high-, medium- and low-dose groups, respectively. Key biomarkers of RF, identified using metabolomics, were most affected by the medium dose. BUT extract displays a protective effect on RF in rats and should be investigated as a candidate drug for the treatment of the disease.

Escherichia coli has been engineered to produce isobutanol, with titers reaching greater than the toxicity level. However, the specific effects of isobutanol on the cell have never been fully understood. Here, we aim to identify genotype–phenotype relationships in isobutanol response. An isobutanol‐tolerant mutant was isolated with serial transfers. Using whole‐genome sequencing followed by gene repair and knockout, we identified five mutations ( acrA , gatY , tnaA , yhbJ , and marCRAB ) that were primarily responsible for the increased isobutanol tolerance. We successfully reconstructed the tolerance phenotype by combining deletions of these five loci, and identified glucosamine‐6‐phosphate as an important metabolite for isobutanol tolerance, which presumably enhanced membrane synthesis. The isobutanol‐tolerant mutants also show increased tolerance to n ‐butanol and 2‐methyl‐1‐butanol, but showed no improvement in ethanol tolerance and higher sensitivity to hexane and chloramphenicol than the parental strain. These results suggest that C4, C5 alcohol stress impacts the cell differently compared with the general solvent or antibiotic stresses. Interestingly, improved isobutanol tolerance did not increase the final titer of isobutanol production.

Rice plants are important food crops that are sensitive to cold stress. Microtubules (MTs) are highly associated with plant response to cold stress. The exogenous application of abscisic acid (ABA) can transiently induce the cold stability of microtubules. These phenotypes were accompanied by the transient increase in Phospholipase D (PLD) enzyme activity. The analysis of detyrosinated/tyrosinated α-tubulin by Western blot in the NtTUA3 line or in the NtTUA3+OsTTL line gave us such a conclusion that the effect of ABA on detyrosinated α-tubulin not only was regulated by ABA but also was dependent on the TTLL12 protein. The dual ABA and 1% n-butanol treatments had shown that ABA-induced detyrosinated α-tubulin in a manner distinct from the n-butanol pathway. Detecting the detyrosinated α-tubulin level after pre-treatment with pertussis toxin (PTX), a G-protein inhibitor, followed by ABA, as well as mastoparan (Mas7) treatment suggested that the effect of ABA on detyrosinated α-tubulin was dependent on PLD activity.

Sleep deprivation due to present-day lifestyle and late-hours work commitments are associated with a broad spectrum of neurobehavioral complications. Moreover, women, as they age, become prone to the cumulative effects of menopause such as sleep disturbances, adiposity, and inflammation which are attributed to a compromised immuno-neuro-endocrine axis. So far, no effective therapeutic remedy is available to mitigate the adverse effects of SD. The current study was aimed to elucidate the neuroprotective potential of n-Butanol fraction obtained from hydroalcoholic extract of Tinospora cordifolia stem (B-TCE). Four groups of female rats are (1) Vehicle-undisturbed sleep, (2) Vehicle-sleep deprived (between 6 a.m. and 6 p.m.), (3) B-TCE oral feeding for 2 weeks and sleep deprivation, and (4) B-TCE alone undisturbed sleep group. Novel Object Recognition test was used to study cognitive impairments and Rotarod for motor coordination. Rats were then sacrificed to study the expression of various marker proteins in the hippocampus and piriform cortex regions of the brain by western blotting. SD was observed to impair the exploratory behavior and neuromuscular coordination, whereas, B-TCE pre-treatment was observed to ameliorate these behavioral functions’- impairments and further suppressed the changes in the expression of markers for synaptic plasticity, inflammation, cell survival, and apoptosis pathways. The current data suggest that B-TCE may be effective in the management of acute SD-associated impairments in learning and memory functions and neuromuscular coordination.

n-Butanol is an essential chemical intermediate produced through microbial fermentation. However, its toxicity to microbial cells has limited its production to a great extent. The anaerobe lactic acid bacteria (LAB) are the most resistant to n-butanol, so it should be the first choice for improving n-butanol production. The present article aims to review the following aspects of n-butanol production by LAB: (1) the tolerance of LAB to n-butanol, including its tolerance level and potential tolerance mechanisms; (2) genome editing tools in the n-butanol-resistant LAB; (3) methods of LAB modification for n-butanol production and the production levels after modification. This review will provide a theoretical basis for further research on n-butanol production by LAB.

Isobutanol has emerged as a potential biofuel due to recent metabolic engineering efforts. Here we used gene expression and transcription network connectivity data, genetic knockouts, and network component analysis (NCA) to map the initial isobutanol response network of Escherichia coli under aerobic conditions. NCA revealed profound perturbations to respiration. Further investigation showed ArcA as an important mediator of this response. Quinone/quinol malfunction was postulated to activate ArcA, Fur, and PhoB in this study. In support of this hypothesis, quinone‐linked ArcA and Fur target expressions were significantly less perturbed by isobutanol under fermentative growth whereas quinol‐linked PhoB target expressions remained activated, and isobutanol impeded growth on glycerol, which requires quinones, more than on glucose. In addition, ethanol, n ‐butanol, and isobutanol response networks were compared. n ‐Butanol and isobutanol responses were qualitatively similar, whereas ethanol had notable induction differences of pspABCDE and ndh , whose gene products manage proton motive force. The network described here could aid design and comprehension of alcohol tolerance, whereas the approach provides a general framework to characterize complex phenomena at the systems level. Synopsis Isobutanol has emerged as a new biofuel owing to the recent metabolic engineering of Escherichia coli for higher branched‐chain alcohol production (Atsumi et al , 2008 ). However, this compound, like other alcohol‐based biofuels, such as n‐butanol and ethanol, is toxic to microorganisms at low concentrations. As this compound was previously considered a minor microbial fermentation product, isobutanol cytotoxicity remains largely uncharacterized. Thus, to facilitate improved isobutanol production a greater understanding of isobutanol stress is desirable. In this paper, we used gene expression and transcription factor (TF)‐gene interaction data (Gama‐Castro et al , 2008 ), genetic knockouts (Baba et al , 2006 ), and network component analysis (NCA) (Liao et al , 2003 ; Tran et al , 2005 ; Yang et al , 2005 ; Galbraith et al , 2006 ) to map the isobutanol response network of Escherichia coli under aerobic conditions. Using NCA and transcription network connectivity to analyze gene expression data from isobutanol stressed cultures, we were able to identify 16 transcription factors with perturbed activity. Out of these, ArcA was most significantly perturbed by isobutanol. To experimentally verify that ArcA modulates gene expression in response to isobutanol, transcriptome measurements were obtained from a Δ arcA strain treated with and without 1% isobutanol. The majority of ArcA‐regulon members perturbed by isobutanol in wild type (47 out of 86) had significantly different expression ratios in Δ arcA . This provided additional evidence that ArcA participates in the E. coli response to isobutanol. The remaining 39 regulon members showed indistinguishable activation/repression in response to isobutanol in Δ arcA compared with wild type. This could have resulted from the inherent noise of DNA microarrays, compensatory action by other regulators, or expression of that gene being under the control of a different TF under isobutanol stress. With ArcA verified by knockout to be involved in the isobutanol response, we sought to identify the upstream isobutanol target responsible for ArcA activation. ArcA is activated through phosphorylation by ArcB, a membrane protein. This phosphorylation occurs after quinone (primarily ubiquinone) inhibition of ArcB autophosphorylation is released. Therefore, given this two‐component mechanism, the likely target for isobutanol is quinone function. To support this hypothesis, we tested the effect of isobutanol on metabolic processes that require quinones. One such example is glycerol degradation, which requires quinones for the glycerol 3‐phosphate dehydrogenase reaction. Figure 3A shows the glycolytic entry pathways for glucose and glycerol under normal aerobic growth conditions. Quinones are the only components of the respiratory chain found along the glycolytic separation of glycerol and glucose. As glycerol directly requires functional quinones to enter glycolysis and glucose does not, growth on glycerol should show more significant retardation than growth on glucose if isobutanol causes quinone malfunction. Growth curves were measured for E. coli in glycerol and glucose minimal media over a spectrum of isobutanol concentrations, and Figure 3B shows the relative time to four doublings from these experiments. These results show that isobutanol hinders growth on glycerol more significantly than growth on glucose, and that this effect becomes more pronounced at higher concentrations of isobutanol. This result supports the hypothesis that isobutanol causes the loss of quinone function, and shows possible repercussions of these findings for isobutanol production in terms of carbon‐source selection. As additional evidence that quinone function mediates isobutanol ArcA activation, we measured the expression of two ArcA‐regulated genes ( sdhC and oppA ), under fermentative conditions using quantitative real‐time PCR. Fermentative conditions were used because ubiquinone is a component of the respiratory chain, and not needed during fermentation. Thus, if the hypothesis is true, ArcA activity will not change in response to isobutanol under fermentative conditions. The expression changes of sdhC an oppA in response to isobutanol, under fermentative conditions were negligible compared with their expression changes in an aerobic environment, and thus further support our hypothesis that quinone malfunction activates ArcA in response to isobutanol. With the profound effect quinone malfunction has on ArcA, we sought to identify additional TFs whose activities were perturbed by isobutanol through quinone malfunction. The activation of PhoB was linked to malfunction of quinol (reduced quinone) regulatory capability, and the activation of Fur was linked to malfunction of quinone electron‐carrier capability. Figure 6 illustrates the isobutanol response network‐associated with quinone malfunction. Quinone has an important role in respiration, and their isobutanol‐associated malfunction alters the respiratory machinery (TCA cycle, glyoxolate shunt, cytochromes, NADH dehydrogenases) as well as iron and phosphate homeostasis. On isobutanol treatment, ArcB senses a decrease in respiratory performance and activates its two‐component‐system partner ArcA, which adjusts cellular metabolism for growth with decreased respiratory efficiency (e.g. low oxygen). This decrease in respiratory performance results in reductive stress from an increase in the NADH/NAD + and a decrease in endogenous O 2 − . Fur senses this reductive stress and represses genes associated with iron uptake in preparation for conditions where Fe–S clusters are safe from damage by reactive oxygen species. PhoR senses a disruption in quinol inhibition by isobutanol and activates its two‐component‐system partner PhoB, which could signal a shift to an environment with higher phosphate demand. In addition, ethanol, n‐butanol, and isobutanol response networks were compared. N‐butanol and isobutanol responses were qualitatively similar, whereas ethanol had notable induction differences of pspABCDE and ndh , whose gene products manage proton motive force (PMF). It is thought that the psp gene products act to restore PMF lost due to environmental stress (Darwin, 2005 ), whereas ndh encodes NADH dehydrogenase II, which is thought to manage redox state when the capacity to generate energy is greater than demand (Calhoun et al , 1993 ; Jackson et al , 2004 ). These results imply that one of the most important membrane‐associated processes, generation and regulation of PMF, is handled differently by E.coli under ethanol stress compared to n‐butanol and isobutanol. The results presented here connect changes in respiratory, phosphate, and iron control to the malfunction of a single class of membrane components on exposure to isobutanol stress. The network described here could aid isobutanol production through the design and comprehension of alcohol tolerance, whereas the approach provides a general framework to characterize complex phenomena at the systems level. Isobutanol, a potential biofuel, activates the transcription factors ArcA, Fur, and PhoB in Escherichia coli ArcA, Fur, and PhoB activations are caused by disruption of quinone function Growth on glycerol is more significantly retarded by isobutanol than growth on glucose, and this can be predicted by the dependence of these carbon sources on quinone function Isobutanol and n‐butanol response networks are qualitatively the same, while ethanol has notable induction differences of genes related to management of proton motive force, and this difference is mediated by the transcription factor, IHF