scholarly journals Acidithiobacillus caldus Sulfur Oxidation Model Based on Transcriptome Analysis between the Wild Type and Sulfur Oxygenase Reductase Defective Mutant

PLoS ONE ◽  
2012 ◽  
Vol 7 (9) ◽  
pp. e39470 ◽  
Author(s):  
Linxu Chen ◽  
Yilin Ren ◽  
Jianqun Lin ◽  
Xiangmei Liu ◽  
Xin Pang ◽  
...  
Keyword(s):  
Transcriptome Analysis ◽  
Sulfur Oxidation ◽  
Wild Type ◽  
Model Based ◽  
Acidithiobacillus Caldus ◽  
Defective Mutant ◽  
Oxidation Model ◽  
Sulfur Oxygenase Reductase

Sulfur Oxygenase Reductase in Different Acidithiobacillus Caldus-Like Strains

2009 ◽  
Vol 71-73 ◽  
pp. 239-242 ◽  
Author(s):  
Claudia Janosch ◽  
Christian Thyssen ◽  
Mario A. Vera ◽  
Violaine Bonnefoy ◽  
Thore Rohwerder ◽  
...  
Keyword(s):  
Elemental Sulfur ◽  
Elevated Temperatures ◽  
Sulfur Oxidation ◽  
Aquifex Aeolicus ◽  
Acidithiobacillus Caldus ◽  
Acidophilic Bacteria ◽  
Cell Extracts ◽  
Moderate Thermophile ◽  
Acidianus Brierleyi ◽  
Sulfur Oxygenase Reductase

The elemental sulfur oxidising enzyme Sulfur Oxygenase Reductase (SOR) is very well investigated in acidothermophilic archaea, such as Acidianus brierleyi and Sulfolobus metallicus. In contrast, not much is known about the biochemistry of elemental sulfur oxidation in acidophilic bacteria. Recently, however, the SOR-encoding gene has been found also in a bacterial strain closely related to the moderate thermophile Acidithiobacillus caldus. Confusingly, for the latter species, also the involvement of the SOX system as well as thiosulfate:quinone oxidoreductase (TQO) and tetrathionate hydrolase (TTH) in sulfur compound oxidation has been proposed based on genome analysis. In this study, we have detected the sor-gene in other Acidithiobacillus caldus-like strains, isolated from various bioleaching habitats, indicating that SOR plays an important role in sulfur oxidation in this species. Based on sequence comparison, the new bacterial sor-genes are closely related and distant from the known archaeal sequences as well as from the SOR found in the neutrophilic bacterium Aquifex aeolicus. In addition, SOR activity has been detected in crude cell extracts from all Acidithiobacillus caldus-like strains tested. The enzyme is truly thermophilic as highest activities were achieved at 65 °C, which is far beyond the growth optimum of Acidithiobacillus caldus. This finding may give rise to the question whether the presence of SOR in Acidithiobacillus caldus is only relevant while growing at elevated temperatures. Currently, experiments are performed for testing this hypothesis (comparing growth and enzyme activities at 30 vs. 45 °C).

scholarly journals Transcriptome Analysis Provides Insights into the Mechanism of Astaxanthin Enrichment in a Mutant of the Ridgetail White Prawn Exopalaemon carinicauda

Genes ◽  
2021 ◽  
Vol 12 (5) ◽  
pp. 618
Author(s):  
Yue Jin ◽  
Shihao Li ◽  
Yang Yu ◽  
Chengsong Zhang ◽  
Xiaojun Zhang ◽  
...  
Keyword(s):  
Transcriptome Analysis ◽  
Underlying Mechanism ◽  
Biological Processes ◽  
Wild Type ◽  
Expression Levels ◽  
In The Wild ◽  
Cuticle Proteins ◽  
Apolipoprotein D ◽  
High Level ◽  
Lower Expression

A mutant of the ridgetail white prawn, which exhibited rare orange-red body color with a higher level of free astaxanthin (ASTX) concentration than that in the wild-type prawn, was obtained in our lab. In order to understand the underlying mechanism for the existence of a high level of free astaxanthin, transcriptome analysis was performed to identify the differentially expressed genes (DEGs) between the mutant and wild-type prawns. A total of 78,224 unigenes were obtained, and 1863 were identified as DEGs, in which 902 unigenes showed higher expression levels, while 961 unigenes presented lower expression levels in the mutant in comparison with the wild-type prawns. Based on Gene Ontology analysis and Kyoto Encyclopedia of Genes and Genomes analysis, as well as further investigation of annotated DEGs, we found that the biological processes related to astaxanthin binding, transport, and metabolism presented significant differences between the mutant and the wild-type prawns. Some genes related to these processes, including crustacyanin, apolipoprotein D (ApoD), cathepsin, and cuticle proteins, were identified as DEGs between the two types of prawns. These data may provide important information for us to understand the molecular mechanism of the existence of a high level of free astaxanthin in the prawn.

scholarly journals Transcriptome analyses of 7-day-old zebrafish larvae possessing a familial Alzheimer’s disease-like mutation in psen1 indicate effects on oxidative phosphorylation, ECM and MCM functions, and iron homeostasis

BMC Genomics ◽  
2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Yang Dong ◽  
Morgan Newman ◽  
Stephen M. Pederson ◽  
Karissa Barthelson ◽  
Nhi Hin ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Oxidative Phosphorylation ◽  
Transcriptome Analysis ◽  
Iron Homeostasis ◽  
Late Onset ◽  
Wild Type ◽  
Familial Alzheimer’S Disease ◽  
Zebrafish Larvae ◽  
Familial Alzheimer's Disease

Abstract Background Early-onset familial Alzheimer’s disease (EOfAD) is promoted by dominant mutations, enabling the study of Alzheimer’s disease (AD) pathogenic mechanisms through generation of EOfAD-like mutations in animal models. In a previous study, we generated an EOfAD-like mutation, psen1Q96_K97del, in zebrafish and performed transcriptome analysis comparing entire brains from 6-month-old wild type and heterozygous mutant fish. We identified predicted effects on mitochondrial function and endolysosomal acidification. Here we aimed to determine whether similar effects occur in 7 day post fertilization (dpf) zebrafish larvae that might be exploited in screening of chemical libraries to find ameliorative drugs. Results We generated clutches of wild type and heterozygous psen1Q96_K97del 7 dpf larvae using a paired-mating strategy to reduce extraneous genetic variation before performing a comparative transcriptome analysis. We identified 228 differentially expressed genes and performed various bioinformatics analyses to predict cellular functions. Conclusions Our analyses predicted a significant effect on oxidative phosphorylation, consistent with our earlier observations of predicted effects on ATP synthesis in adult heterozygous psen1Q96_K97del brains. The dysregulation of minichromosome maintenance protein complex (MCM) genes strongly contributed to predicted effects on DNA replication and the cell cycle and may explain earlier observations of genome instability due to PSEN1 mutation. The upregulation of crystallin gene expression may be a response to defective activity of mutant Psen1 protein in endolysosomal acidification. Genes related to extracellular matrix (ECM) were downregulated, consistent with previous studies of EOfAD mutant iPSC neurons and postmortem late onset AD brains. Also, changes in expression of genes controlling iron ion transport were observed without identifiable changes in the prevalence of transcripts containing iron responsive elements (IREs) in their 3′ untranslated regions (UTRs). These changes may, therefore, predispose to the apparent iron dyshomeostasis previously observed in 6-month-old heterozygous psen1Q96_K97del EOfAD-like mutant brains.

scholarly journals Syntaxin-17-Dependent Mitochondrial Dynamics is Essential for Protection Against Oxidative-Stress-Induced Apoptosis

Antioxidants ◽  
2019 ◽  
Vol 8 (11) ◽  
pp. 522 ◽  
Author(s):  
Wang ◽  
Xiao ◽  
Huang ◽  
Liu
Keyword(s):  
Oxidative Stress ◽  
Mitochondrial Dynamics ◽  
Mitochondrial Fission ◽  
Autophagic Flux ◽  
Wild Type ◽  
Dual Roles ◽  
Defective Mutant ◽  
U2os Cells ◽  
Induced Apoptosis

In this study, cell death induced by the oxidant tert-butylhydroperoxide (tBH) was observed in U2OS cells; this phenotype was rescued by Syntaxin 17 (STX17) knockout (KO) but the mechanism is unknown. STX17 plays dual roles in autophagosome–lysosome fusion and mitochondrial fission. However, the contribution of the two functions of STX17 to apoptosis has not been extensively studied. Here, we sought to dissect the dual roles of STX17 in oxidative-stress-induced apoptosis by taking advantage of STX17 knockout cells and an autophagosome–lysosome fusion defective mutant of STX17. We generated STX17 knockout U2OS cells using the clustered regularly interspaced short palindromic repeats (CRISPR)/CRISPR-associated protein 9 (Cas9) system and the STX17 knockout cells were reconstituted with wild-type STX17 and its autophagosome–lysosome fusion defective mutant. Autophagy was assessed by autophagic flux assay, Monomer red fluorescent protein (mRFP)–GFP–LC3 assay and protease protection assay. Golgi, endoplasmic reticulum (ER)/ER–Golgi intermediate compartment (ERGIC) and mitochondrial dynamics were examined by staining the different indicator proteins. Apoptosis was evaluated by caspase cleavage assay. The general reactive oxygen species (ROS) were detected by flow cytometry. In STX17 complete knockout cells, sealed autophagosomes were efficiently formed but their fusion with lysosomes was less defective. The fusion defect was rescued by wild-type STX17 but not the autophagosome–lysosome fusion defective mutant. No obvious defects in Golgi, ERGIC or ER dynamics were observed. Mitochondria were significantly elongated, supporting a role of STX17 in mitochondria fission and the elongation caused by STX17 KO was reversed by the autophagosome–lysosome fusion defective mutant. The clearance of protein aggregation was compromised, correlating with the autophagy defect but not with mitochondrial dynamics. This study revealed a mixed role of STX17 in autophagy, mitochondrial dynamics and oxidative stress response. STX17 knockout cells were highly resistant to oxidative stress, largely due to the function of STX17 in mitochondrial fission rather than autophagy.

scholarly journals Plant Hormone Metabolome and Transcriptome Analysis of Dwarf and Wild-type Banana

2021 ◽  
Author(s):  
Biao Deng ◽  
Xuan Wang ◽  
Xing Long ◽  
Ren Fang ◽  
Shuangyun Zhou ◽  
...  
Keyword(s):  
Signal Transduction ◽  
Transcriptome Analysis ◽  
Regulatory Mechanism ◽  
Feedback Regulation ◽  
Wild Type ◽  
Hormone Levels ◽  
Transporter Protein ◽  
Repressor Proteins ◽  
Differential Gene ◽  
The Relationship

AbstractGibberellin (GA), auxin (IAA) and brassinosteroid (BR) are indispensable in the process of plant growth and development. Currently, research on the regulatory mechanism of phytohormones in banana dwarfism is mainly focused on GA, and few studies are focused on IAA and BR. In this study, we measured the contents of endogenous GA, IAA and BR and compared the transcriptomes of wild-type Williams banana and its dwarf mutant across five successive growth periods. We investigated the relationship between hormones and banana dwarfism and explored differential gene expression through transcriptome analysis, thus revealing the possible metabolic regulatory mechanism. We inferred a complex regulatory network of banana dwarfing. In terms of endogenous hormone levels, GA and IAA had significant effects on banana dwarfing, while BR had little effect. The key gene in GA biosynthesis of is GA2ox, and the key genes in IAA biosynthesis are TDC and YUCCA. The differential expression of these genes might be the main factor affecting hormone levels and plant height. In terms of hormone signal transduction, DELLA and AUX/IAA repressor proteins were the core regulators of GA and IAA, respectively. They inhibited the process of signal transduction and had feedback regulation on hormone levels. Finally, the transporter protein PIN, AUX1/LAX protein family and ABCB subfamily played supplementary roles in the transport of IAA. These results provide new insights into GA and IAA regulation of banana growth and a reliable foundation for the improvement of dwarf varieties.

Small deletion in v-src SH3 domain of a transformation defective mutant of rous sarcoma virus restores wild type transforming properties

Virology ◽  
1992 ◽  
Vol 189 (2) ◽  
pp. 556-567 ◽  
Author(s):  
Philippe Dezélée ◽  
Jean Vianney Barnier ◽  
Annie Hampe ◽  
Danielle Laugier ◽  
Maria Marx ◽  
...  
Keyword(s):  
Rous Sarcoma Virus ◽  
Sh3 Domain ◽  
Wild Type ◽  
Small Deletion ◽  
Rous Sarcoma ◽  
Defective Mutant ◽  
Sarcoma Virus

Functional asymmetry of the regions juxtaposed to the membrane-binding sequence of polyomavirus middle T antigen

1992 ◽  
Vol 12 (11) ◽  
pp. 5050-5058
Author(s):  
J Dahl ◽  
U Thathamangalam ◽  
R Freund ◽  
T L Benjamin
Keyword(s):  
Complete Removal ◽  
T Antigen ◽  
Site Directed Mutagenesis ◽  
Wild Type ◽  
Hydrophobic Membrane ◽  
Amino Terminal ◽  
Charged Amino Acids ◽  
Defective Mutant ◽  
Polyomavirus Middle T Antigen ◽  
Membrane Anchoring

The functional importance of the two clusters of positively charged amino acids which flank the hydrophobic membrane-anchoring sequence of polyomavirus middle T (mT) protein has been investigated by using site-directed mutagenesis. A clear asymmetry was apparent. No effect on transformation was seen following multiple alterations or complete removal of the cluster at the carboxyl end of the protein. In contrast, a single substitution replacing the first arginine amino terminal to the hydrophobic stretch with glutamic acid, but not with lysine, histidine, or methionine, produced a partially transformation-defective mutant with a novel phenotype. This mutant failed to confer anchorage-independent growth on F111 established rat embryo fibroblasts but induced foci with altered morphology compared with wild-type mT. Biochemical studies on this mutant revealed that F111 clones expressing levels of mutant mT equivalent to those of wild-type controls showed a 65% reduction in pp60c-src activation and an 87% reduction in mT-associated phosphatidylinositol 3-kinase activity. However, F111 clones expressing seven times more mutant mT than did wild-type controls showed equal or greater levels of kinase activities yet remained incompletely transformed. Possible mechanisms involving this transformation-sensitive region of mT are discussed.

scholarly journals Expanding heterochromatin reveals discrete subtelomeric domains delimited by chromatin landscape transitions

2017 ◽  
Author(s):  
Antoine Hocher ◽  
Myriam Ruault ◽  
Petra Kaferle ◽  
Marc Descrimes ◽  
Mickael Garnier ◽  
...  
Keyword(s):  
Meta Analysis ◽  
Position Effect ◽  
Histone Mark ◽  
Eukaryotic Genome ◽  
Wild Type ◽  
Histone Marks ◽  
The Core ◽  
Defective Mutant ◽  
H3k79 Methylation ◽  
Subtelomeric Regions

AbstractThe eukaryotic genome is divided into chromosomal domains of heterochromatin and euchromatin. Transcriptionally silent heterochromatin is found at subtelomeric regions, leading to the telomeric position effect (TPE) in yeast, fly and man. Heterochromatin generally initiates and spreads from defined loci, and diverse mechanisms prevent the ectopic spread of heterochromatin into euchromatin. Here, we overexpressed the silencing factor Sir3 at various levels in yeast, and found that Sir3 spreading into Extended Silent Domains (ESD) eventually reached saturation at subtelomeres. We observed that Sir3 spreading into ESDs covered zone associated with specific histone marks in wild-type cells and stopped at zones of histone mark transitions including H3K79 tri-methylation levels. The conserved enzyme Dot1 deposits H3K79 methylation, and we found that it is essential for viability upon overexpression of Sir3, but not of a spreading-defective mutant Sir3A2Q. These data suggest that H3K79 methylation actively blocks Sir3 spreading. Lastly, our meta-analysis uncovers previously uncharacterized discrete subtelomeric domains associated with specific chromatin features offering a new viewpoint on how to separate subtelomeres from the core chromosome.

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