scholarly journals Detoxification and Transcriptome Response in Arabidopsis Seedlings Exposed to the Allelochemical Benzoxazolin-2(3H)-one

2005 ◽  
Vol 280 (23) ◽  
pp. 21867-21881 ◽  
Author(s):  
Scott R. Baerson ◽  
Adela Sánchez-Moreiras ◽  
Nuria Pedrol-Bonjoch ◽  
Margot Schulz ◽  
Isabelle A. Kagan ◽  
...  

Benzoxazolin-2(3H)-one (BOA) is an allelochemical most commonly associated with monocot species, formed from the O-glucoside of 2,4-dihydroxy-2H-1,4-benzoxazin-3(4H)-one by a two-step degradation process. The capacity of Arabidopsis to detoxify exogenously supplied BOA was analyzed by quantification of the major known metabolites BOA-6-OH, BOA-6-O-glucoside, and glucoside carbamate, revealing that detoxification occurs predominantly through O-glucosylation of the intermediate BOA-6-OH, most likely requiring the sequential action of as-yet-unidentified cytochrome P450 and UDP-glucosyltransferase activities. Transcriptional profiling experiments were also performed with Arabidopsis seedlings exposed to BOA concentrations, representing I50 and I80 levels based on root elongation inhibition assays. One of the largest functional categories observed for BOA-responsive genes corresponded to protein families known to participate in cell rescue and defense, with the majority of these genes potentially associated with chemical detoxification pathways. Further experiments using a subset of these genes revealed that many are also transcriptionally induced by a variety of structurally diverse xenobiotic compounds, suggesting they comprise components of a coordinately regulated, broad specificity xenobiotic defense response. The data significantly expand upon previous studies examining plant transcriptional responses to allelochemicals and other environmental toxins and provide novel insights into xenobiotic detoxification mechanisms in plants.

Author(s):  
Xia Zhang ◽  
Brayden Weir ◽  
Hongru Wei ◽  
Zhiwei Deng ◽  
Xiaoqi Zhang ◽  
...  

AbstractChickpea is an economically important legume crop with high nutritional value in human diets. Aluminium-toxicity poses a significant challenge for the yield improvement of this increasingly popular crop in acidic soils. The wild progenitors of chickpea may provide a more diverse gene pool for Al-tolerance in chickpea breeding. However, the genetic basis of Al-tolerance in chickpea and its wild relatives remains largely unknown. Here, we assessed the Al-tolerance of six selected wild Cicer accessions by measuring the root elongation in solution culture under control (0 µM Al3+) and Al-treatment (30 µM Al3+) conditions. Al-treatment significantly reduced the root elongation in all target lines compared to the control condition after 2-day’s growth. However, the relative reduction of root elongation in different lines varied greatly: 3 lines still retained significant root growth under Al-treatment, whilst another 2 lines displayed no root growth at all. We performed genome-wide identification of multidrug and toxic compound extrusion (MATE) encoding genes in the Cicer genome. A total of 56 annotated MATE genes were identified, which divided into 4 major phylogeny groups (G1-4). Four homologues to lupin LaMATE (> 50% aa identity; named CaMATE1-4) were clustered with previously characterised MATEs related to Al-tolerance in various other plants. qRT-PCR showed that CaMATE2 transcription in root tips was significantly up-regulated upon Al-treatment in all target lines, whilst CaMATE1 was up-regulated in all lines except Bari2_074 and Deste_064, which coincided with the lines displaying no root growth under Al-treatment. Transcriptional profiling in five Cicer tissues revealed that CaMATE1 is specifically transcribed in the root tissue, further supporting its role in Al-detoxification in roots. This first identification of MATE-encoding genes associated with Al-tolerance in Cicer paves the ways for future functional characterization of MATE genes in Cicer spp., and to facilitate future design of gene-specific markers for Al-tolerant line selection in chickpea breeding programs.


2004 ◽  
Vol 186 (3) ◽  
pp. 866-869 ◽  
Author(s):  
Daniel Walker ◽  
Matthew Rolfe ◽  
Arthur Thompson ◽  
Geoffrey R. Moore ◽  
Richard James ◽  
...  

ABSTRACT We report the transcriptional response of Escherichia coli MG1655 to damage induced by colicins E3 and E9, bacteriocins that kill cells through inactivation of the ribosome and degradation of chromosomal DNA, respectively. Colicin E9 strongly induced the LexA-regulated SOS response, while colicin E3 elicited a broad response that included the induction of cold shock genes, symptomatic of translational arrest. Colicin E3 also increased the transcription of cryptic prophage genes and other laterally acquired mobile elements. The transcriptional responses to both these toxins suggest mechanisms that may promote genetic diversity in E. coli populations, pointing to a more general role for colicins in adaptive bacterial physiology than has hitherto been realized.


2004 ◽  
Vol 72 (12) ◽  
pp. 7247-7256 ◽  
Author(s):  
Samithamby Jeyaseelan ◽  
Hong Wei Chu ◽  
Scott K. Young ◽  
G. Scott Worthen

ABSTRACT Mortality associated with acute lung injury (ALI) induced by lipopolysaccharide (LPS) remains high in humans, warranting improved treatment and prevention strategies. ALI is characterized by the expression of proinflammatory mediators and extensive neutrophil influx into the lung, followed by severe lung damage. Understanding the pathogenesis of LPS-induced ALI is a prerequisite for designing better therapeutic strategies. In the present study, we used microarrays to gain a global view of the transcriptional responses of the lung to LPS in a mouse model of ALI that mimics ALI in humans. A total of 71 inflammation-associated genes were up-regulated in LPS-treated lungs, including a chemokine, LPS-induced CXC chemokine (LIX), whose role in the induction of ALI is unknown. Most of the inflammatory genes peaked at 2 h post-LPS treatment. Real-time reverse transcription-PCR confirmed the LPS-induced up-regulation of selected genes identified by microarray analysis, including LIX. The up-regulation of LIX, tumor necrosis factor alpha, and macrophage inflammatory protein 2 was confirmed at the protein level by enzyme-linked immunosorbent assays. To determine the role of LIX in the induction of ALI, we used both exogenous LIX and a LIX blocking antibody. Exogenous LIX alone elicited a neutrophil influx in the lungs, and the anti-LIX antibody attenuated the LPS-induced neutrophil accumulation in the lungs. Taken together, the results of our study demonstrate for the first time the temporal expression of inflammatory genes during LPS-induced ALI and suggest that early therapeutic intervention is crucial to attenuate lung damage. Moreover, we identified a role for LIX in the induction of ALI, and therefore LIX may serve as a novel therapeutic target for the minimization of ALI.


2002 ◽  
Vol 10 (2) ◽  
pp. 103-111 ◽  
Author(s):  
Jennifer L. Moran ◽  
Yizheng Li ◽  
Andrew A. Hill ◽  
William M. Mounts ◽  
Christopher P. Miller

Studies described here utilize high-density oligonucleotide arrays to characterize changes in global mRNA expression patterns during proliferation, cell cycle withdrawal, and terminal differentiation in mouse C2C12 myoblasts. Statistical analyses revealed 629 sequences differentially regulated between proliferating and differentiating myoblasts. These genes were clustered using self-organizing maps to identify sets of coregulated genes and were assigned to functional categories that were analyzed for distribution across expression clusters. Clusters were identified with statistically significant enrichment of functional categories including muscle contraction, cell adhesion, extracellular matrix function, cellular metabolism, mitochondrial transport, DNA replication, cell cycle control, mRNA transcription, and unexpectedly, immune regulation. In addition, functional category enrichment data can be used to predict gene function for numerous differentially regulated expressed sequence tags. The results provide new insight into how genes involved in these cellular processes may play a role in skeletal muscle growth and differentiation.


2016 ◽  
Vol 82 (6) ◽  
pp. 1933-1944 ◽  
Author(s):  
Hong Zhou ◽  
Xia Wang ◽  
Tengteng Yang ◽  
Weixin Zhang ◽  
Guanjun Chen ◽  
...  

ABSTRACTCytophaga hutchinsoniispecializes in cellulose digestion by employing a collection of novel cell-associated proteins. Here, we identified a novel gene locus, CHU_1276, that is essential forC. hutchinsoniicellulose utilization. Disruption of CHU_1276 inC. hutchinsoniiresulted in complete deficiency in cellulose degradation, as well as compromised assimilation of cellobiose or glucose at a low concentration. Further analysis showed that CHU_1276 was an outer membrane protein that could be induced by cellulose and low concentrations of glucose. Transcriptional profiling revealed that CHU_1276 exerted a profound effect on the genome-wide response to both glucose and Avicel and that the mutant lacking CHU_1276 displayed expression profiles very different from those of the wild-type strain under different culture conditions. Specifically, comparison of their transcriptional responses to cellulose led to the identification of a gene set potentially regulated by CHU_1276. These results suggest that CHU_1276 plays an essential role in cellulose utilization, probably by coordinating the extracellular hydrolysis of cellulose substrate with the intracellular uptake of the hydrolysis product inC. hutchinsonii.


2021 ◽  
Author(s):  
Wendong Kuang ◽  
Chenghua Yan ◽  
Zhigao Zhan ◽  
Limei Guan ◽  
Jinchang Wang ◽  
...  

Abstract Background: Daphnis nerii cypovirus-23 (DnCPV-23) is a new type of cypovirus and has lethal effect on the oleander hawk moth, Daphnis nerii , which feeds on leave of Oleander and Catharanthus et al. After DnCPV-23 infection, the change of Daphnis nerii responses has not been reported.Methods: In order to better understand the pathogenic mechanism of DnCPV-23 infection, 3rdinstar Daphnis nerii larvae were orally infected with DnCPV-23 occlusion bodies and the transcriptional responses of the Daphnis nerii midgut were analyzed 72 h post-infection using RNA-seq.Results: The results showed that 1,979 differentially expressed Daphnis nerii transcripts in the infected midgut had been identified. KEGG analysis showed that protein digestion and absorption, Toll and Imd signaling pathway were down-regulated. Based on the result, it was possible the function of food digestion and absorption in insect midgut was impaired after virus infection. In addition, the down-regulation of the immune response may be conducive to viral immune escape. Glycerophospholipid metabolism and xenobiotics metabolism were up-regulated. These two types of pathways may affect the viral replication and xenobiotic detoxification of insect, respectively. Conclusion: These results may facilitate a better understanding of the changes in Daphnis nerii metabolism during cypovirus infection and serve as a basis for future research on the molecular mechanism of DnCPV-23 invasion.


2019 ◽  
Author(s):  
Sung Rye Park ◽  
Sim Namkoong ◽  
Zac Zezhi Zhang ◽  
Leon Friesen ◽  
Yu-Chih Chen ◽  
...  

Cancer cells often heterogeneously respond to genotoxic chemotherapy, leading to fractional killing and chemoresistance1, 2, which remain as the major obstacles in cancer treatment. It is widely believed that DNA damage induces a uniform response in regulating transcription and that cell fate is passively determined by a threshold mechanism evaluating the level of transcriptional responses3. On the contrary to this assumption, here we show that a surprisingly high level of heterogeneity exists in individual cell transcriptome responses to DNA damage, and that these transcriptome variations dictate the cell fate after DNA damage. Many DNA damage response genes, including tumor suppressor p53 targets, were exclusively expressed in only a subset of cells having specific cell fate, producing unique stress responses tailored for the fate that the cells are committed to. For instance, CDKN1A, the best known p53 target inhibiting cell cycle, was specifically expressed in a subset of cells undergoing cell cycle checkpoint, while other pro-apoptotic p53 targets were expressed only in cells undergoing apoptosis. A small group of cells exhibited neither checkpoint nor apoptotic responses, but produced a unique transcriptional program that conferred strong chemoresistance to the cells. The heterogeneous transcriptome response to DNA damage was also observed at the protein level in flow cytometry. Our results demonstrate that cell fate heterogeneity after DNA damage is mediated by distinct transcriptional programs generating fate-specific gene expression landscapes. This finding provides an important insight into understanding heterogeneous chemotherapy responses of cancer cells.


2018 ◽  
Vol 115 (8) ◽  
pp. E1749-E1758 ◽  
Author(s):  
Joao G. N. Moraes ◽  
Susanta K. Behura ◽  
Thomas W. Geary ◽  
Peter J. Hansen ◽  
Holly L. Neibergs ◽  
...  

A major unresolved issue is how the uterus influences infertility and subfertility in cattle. Serial embryo transfer was previously used to classify heifers as high-fertile (HF), subfertile (SF), or infertile (IF). To assess pregnancy loss, two in vivo-produced embryos were transferred into HF, SF, and IF heifers on day 7, and pregnancy outcome was assessed on day 17. Pregnancy rate was substantially higher in HF (71%) and SF (90%) than IF (20%) heifers. Elongating conceptuses were about twofold longer in HF than SF heifers. Transcriptional profiling detected relatively few differences in the endometrium of nonpregnant HF, SF, and IF heifers. In contrast, there was a substantial difference in the transcriptome response of the endometrium to pregnancy between HF and SF heifers. Considerable deficiencies in pregnancy-dependent biological pathways associated with extracellular matrix structure and organization as well as cell adhesion were found in the endometrium of SF animals. Distinct gene expression differences were also observed in conceptuses from HF and SF animals, with many of the genes decreased in SF conceptuses known to be embryonic lethal in mice due to defects in embryo and/or placental development. Analyses of biological pathways, key players, and ligand–receptor interactions based on transcriptome data divulged substantial evidence for dysregulation of conceptus–endometrial interactions in SF animals. These results support the ideas that the uterus impacts conceptus survival and programs conceptus development, and ripple effects of dysregulated conceptus–endometrial interactions elicit loss of the postelongation conceptus in SF cattle during the implantation period of pregnancy.


2019 ◽  
Vol 116 (52) ◽  
pp. 26835-26845 ◽  
Author(s):  
Rebecca L. Porter ◽  
Neelima K. C. Magnus ◽  
Vishal Thapar ◽  
Robert Morris ◽  
Annamaria Szabolcs ◽  
...  

Transcriptional profiling has defined pancreatic ductal adenocarcinoma (PDAC) into distinct subtypes with the majority being classical epithelial (E) or quasi-mesenchymal (QM). Despite clear differences in clinical behavior, growing evidence indicates these subtypes exist on a continuum with features of both subtypes present and suggestive of interconverting cell states. Here, we investigated the impact of different therapies being evaluated in PDAC on the phenotypic spectrum of the E/QM state. We demonstrate using RNA-sequencing and RNA-in situ hybridization (RNA-ISH) that FOLFIRINOX combination chemotherapy induces a common shift of both E and QM PDAC toward a more QM state in cell lines and patient tumors. In contrast, Vitamin D, another drug under clinical investigation in PDAC, induces distinct transcriptional responses in each PDAC subtype, with augmentation of the baseline E and QM state. Importantly, this translates to functional changes that increase metastatic propensity in QM PDAC, but decrease dissemination in E PDAC in vivo models. These data exemplify the importance of both the initial E/QM subtype and the plasticity of E/QM states in PDAC in influencing response to therapy, which highlights their relevance in guiding clinical trials.


2007 ◽  
Vol 52 (3) ◽  
pp. 980-990 ◽  
Author(s):  
Arunachalam Muthaiyan ◽  
Jared A. Silverman ◽  
Radheshyam K. Jayaswal ◽  
Brian J. Wilkinson

ABSTRACT Daptomycin is a lipopeptide antibiotic that has recently been approved for treatment of gram-positive bacterial infections. The mode of action of daptomycin is not yet entirely clear. To further understand the mechanism transcriptomic analysis of changes in gene expression in daptomycin-treated Staphylococcus aureus was carried out. The expression profile indicated that cell wall stress stimulon member genes (B. J. Wilkinson, A. Muthaiyan, and R. K. Jayaswal, Curr. Med. Chem. Anti-Infect. Agents 4:259-276, 2005) were significantly induced by daptomycin and by the cell wall-active antibiotics vancomycin and oxacillin. Comparison of the daptomycin response of a two-component cell wall stress stimulon regulator VraSR mutant, S. aureus KVR, to its parent N315 showed diminished expression of the cell wall stress stimulon in the mutant. Daptomycin has been proposed to cause membrane depolarization, and the transcriptional responses to carbonyl cyanide m-chlorophenylhydrazone (CCCP) and nisin were determined. Transcriptional profiles of the responses to these antimicrobial agents showed significantly different patterns compared to those of the cell wall-active antibiotics, including little or no induction of the cell wall stress stimulon. However, there were a significant number of genes induced by both CCCP and daptomycin that were not induced by oxacillin or vancomycin, so the daptomycin transcriptome probably reflected a membrane depolarizing activity of this antimicrobial also. The results indicate that inhibition of peptidoglycan biosynthesis, either directly or indirectly, and membrane depolarization are parts of the mode of action of daptomycin.


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