scholarly journals Diversification of methanogens into hyperalkaline serpentinizing environments through adaptations to minimize oxidant limitation

2020 ◽  
Author(s):  
Elizabeth M. Fones ◽  
Daniel R. Colman ◽  
Emily A. Kraus ◽  
Ramunas Stepanauskas ◽  
Alexis S. Templeton ◽  
...  
Keyword(s):  
Gene Transfer ◽  
Relative Abundance ◽  
Hydrogen Oxidation ◽  
Phylogenetic Analyses ◽  
Gene Content ◽  
Type I ◽  
Type Ii ◽  
Sultanate Of Oman ◽  
Methane Generation ◽  
Hydrogenotrophic Methanogens

AbstractMetagenome assembled genomes (MAGs) and single amplified genomes (SAGs) affiliated with two distinct Methanobacterium lineages were recovered from subsurface fracture waters of the Samail Ophiolite, Sultanate of Oman. Lineage Type I was abundant in waters with circumneutral pH, whereas lineage Type II was abundant in hydrogen rich, hyperalkaline waters. Type I encoded proteins to couple hydrogen oxidation to CO2 reduction, typical of hydrogenotrophic methanogens. Surprisingly, Type II, which branched from the Type I lineage, lacked homologs of two key oxidative [NiFe]-hydrogenases. These functions were presumably replaced by formate dehydrogenases that oxidize formate to yield reductant and cytoplasmic CO2 via a pathway that was unique among characterized Methanobacteria, allowing cells to overcome CO2/oxidant limitation in high pH waters. This prediction was supported by microcosm-based radiotracer experiments that showed significant biological methane generation from formate, but not bicarbonate, in waters where the Type II lineage was detected in highest relative abundance. Phylogenetic analyses and variability in gene content suggested that recent and ongoing diversification of the Type II lineage was enabled by gene transfer, loss, and transposition. These data indicate that selection imposed by CO2/oxidant availability drove recent methanogen diversification into hyperalkaline waters that are heavily impacted by serpentinization.

scholarly journals Functional Metagenomics of a Biostimulated Petroleum-Contaminated Soil Reveals an Extraordinary Diversity of Extradiol Dioxygenases

2016 ◽  
Vol 82 (8) ◽  
pp. 2467-2478 ◽  
Author(s):  
Laura Terrón-González ◽  
Guadalupe Martín-Cabello ◽  
Manuel Ferrer ◽  
Eduardo Santero
Keyword(s):  
Contaminated Soil ◽  
Phylogenetic Analyses ◽  
Metagenomic Library ◽  
Type I ◽  
Type Ii ◽  
Extradiol Dioxygenase ◽  
Metagenomic Dna ◽  
Petroleum Contaminated Soil ◽  
Definition Of ◽  
Extradiol Dioxygenases

ABSTRACTA metagenomic library of a petroleum-contaminated soil was constructed in a fosmid vector that allowed heterologous expression of metagenomic DNA. The library, consisting of 6.5 Gb of metagenomic DNA, was screened for extradiol dioxygenase (Edo) activity using catechol and 2,3-dihydroxybiphenyl as the substrates. Fifty-eight independent clones encoding extradiol dioxygenase activity were identified. Forty-one different Edo-encoding genes were identified. The population of Edo genes was not dominated by a particular gene or by highly similar genes; rather, the genes had an even distribution and high diversity. Phylogenetic analyses revealed that most of the genes could not be ascribed to previously defined subfamilies of Edos. Rather, the Edo genes led to the definition of 10 new subfamilies of type I Edos. Phylogenetic analysis of type II enzymes defined 7 families, 2 of which harbored the type II Edos that were found in this work. Particularly striking was the diversity found in family I.3 Edos; 15 out of the 17 sequences assigned to this family belonged to 7 newly defined subfamilies. A strong bias was found that depended on the substrate used for the screening: catechol mainly led to the detection of Edos belonging to the I.2 family, while 2,3-dihydroxybiphenyl led to the detection of most other Edos. Members of the I.2 family showed a clear substrate preference for monocyclic substrates, while those from the I.3 family showed a broader substrate range and high activity toward 2,3-dihydroxybiphenyl. This metagenomic analysis has substantially increased our knowledge of the existing biodiversity of Edos.

The gene transfer of soluble VEGF type I receptor (Flt-1) attenuates peritoneal fibrosis formation in mice but not soluble TGF-β type II receptor gene transfer

2005 ◽  
Vol 288 (1) ◽  
pp. G143-G150 ◽  
Author(s):  
Y. Motomura ◽  
H. Kanbayashi ◽  
W. I. Khan ◽  
Y. Deng ◽  
P. A. Blennerhassett ◽  
...  
Keyword(s):  
Growth Factor ◽  
Gene Transfer ◽  
Negative Correlation ◽  
Significant Negative Correlation ◽  
Receptor Type ◽  
Type I ◽  
Type Ii ◽  
Collagen Deposition ◽  
Significant Elevation ◽  
Peritoneal Fibrosis

Peritoneal fibrosis formation is a consequence of inflammation/injury and a significant medical problem to be solved. The effects of soluble VEGF receptor type I (sFlt-1) gene transfer on experimental peritoneal fibrosis were examined and compared with soluble transforming growth factor-β (TGF-β) receptor type II (sTGFβRII) gene transfer. Male C57BL/6 mice were injected with 1.5 × 108plaque-forming unit of adenovirus encoding active TGF-β (AdTGFβ) intraperitoneally. Some mice had been treated with sTGFβRII or sFlt-1 plasmid injection into skeletal muscle with electroporation 4 days before virus administration. Mice were euthanized at day 14 after virus administration. AdTGFβ induced significant elevation of serum active TGF-β, caused significant inflammatory response [weight loss, elevation of serum amyloid-P (SAP) and IL-12, increased expression of monocyte chemoattractant protein-1 (MCP-1) mRNA], and induced marked thickening of the peritoneum and collagen deposition. Gene transfer of sFlt-1 reduced the collagen deposition ∼81% in mesenteric tissue. Treatment with sFlt-1 decreased ICAM-1 and MCP-1 mRNA expression significantly. Significant negative correlation between serum sFlt-1 and placental growth factor level was observed, whereas there was no significant negative correlation between sFlt-1 and VEGF. On the other hand, sTGFβRII treatment enhanced the AdTGFβ-induced inflammation (significant elevation of SAP, TNF-α, and IL-12 levels and upregulation of ICAM-1 and MCP-1 mRNA expressions) and failed to prevent collagen deposition. These observations indicate that sFlt-1 gene transfer might be of therapeutic benefit in peritoneal fibrosis.

Chaperones and protein folding in the archaea

2009 ◽  
Vol 37 (1) ◽  
pp. 46-51 ◽  
Author(s):  
Andrew T. Large ◽  
Martin D. Goldberg ◽  
Peter A. Lund
Keyword(s):  
Protein Folding ◽  
Heat Shock ◽  
Gene Transfer ◽  
Horizontal Gene Transfer ◽  
Heat Shock Protein ◽  
Haloferax Volcanii ◽  
Functional Specialization ◽  
Type I ◽  
Type Ii ◽  
Shock Proteins

A survey of archaeal genomes for the presence of homologues of bacterial and eukaryotic chaperones reveals several interesting features. All archaea contain chaperonins, also known as Hsp60s (where Hsp is heat-shock protein). These are more similar to the type II chaperonins found in the eukaryotic cytosol than to the type I chaperonins found in bacteria, mitochondria and chloroplasts, although some archaea also contain type I chaperonin homologues, presumably acquired by horizontal gene transfer. Most archaea contain several genes for these proteins. Our studies on the type II chaperonins of the genetically tractable archaeon Haloferax volcanii have shown that only one of the three genes has to be present for the organisms to grow, but that there is some evidence for functional specialization between the different chaperonin proteins. All archaea also possess genes for prefoldin proteins and for small heat-shock proteins, but they generally lack genes for Hsp90 and Hsp100 homologues. Genes for Hsp70 (DnaK) and Hsp40 (DnaJ) homologues are only found in a subset of archaea. Thus chaperone-assisted protein folding in archaea is likely to display some unique features when compared with that in eukaryotes and bacteria, and there may be important differences in the process between euryarchaea and crenarchaea.

Adenoviral mediated gene transfer of PDGF-B enhances wound healing in type I and type II diabetic wounds

2004 ◽  
Vol 12 (5) ◽  
pp. 497-504 ◽  
Author(s):  
Sundeep G. Keswani ◽  
Anna B. Katz ◽  
Foong-Yen Lim ◽  
Philip Zoltick ◽  
Antoneta Radu ◽  
...  
Keyword(s):  
Wound Healing ◽  
Gene Transfer ◽  
Type I ◽  
Type Ii ◽  
Diabetic Wounds

scholarly journals Phylogenetic and Structural Comparisons of the Three Types of Methyl Coenzyme M Reductase from Methanococcales and Methanobacteriales

2017 ◽  
Vol 199 (16) ◽  
Author(s):  
Tristan Wagner ◽  
Carl-Eric Wegner ◽  
Jörg Kahnt ◽  
Ulrich Ermler ◽  
Seigo Shima
Keyword(s):  
Active Site ◽  
Phylogenetic Analyses ◽  
Methanogenic Archaea ◽  
Methane Formation ◽  
Type I ◽  
Type Ii ◽  
Coenzyme M ◽  
Content Type ◽  
Type Iii ◽  
Methyl Coenzyme M Reductase

ABSTRACT The phylogenetically diverse family of methanogenic archaea universally use methyl coenzyme M reductase (MCR) for catalyzing the final methane-forming reaction step of the methanogenic energy metabolism. Some methanogens of the orders Methanobacteriales and Methanococcales contain two isoenzymes. Comprehensive phylogenetic analyses on the basis of all three subunits grouped MCRs from Methanobacteriales and Methanococcales into three distinct types: (i) MCRs from Methanobacteriales, (ii) MCRs from Methanobacteriales and Methanococcales, and (iii) MCRs from Methanococcales. The first and second types contain MCR isoenzymes I and II from Methanothermobacter marburgensis, respectively; therefore, they were designated MCR type I and type II and accordingly; the third one was designated MCR type III. For comparison with the known MCR type I and type II structures, we determined the structure of MCR type III from Methanotorris formicicus and Methanothermococcus thermolithotrophicus. As predicted, the three MCR types revealed highly similar overall structures and virtually identical active site architectures reflecting the chemically challenging mechanism of methane formation. Pronounced differences were found at the protein surface with respect to loop geometries and electrostatic properties, which also involve the entrance of the active-site funnel. In addition, the C-terminal end of the γ-subunit is prolonged by an extra helix after helix γ8 in MCR type II and type III, which is, however, differently arranged in the two MCR types. MCR types I, II, and III share most of the posttranslational modifications which appear to fine-tune the enzymatic catalysis. Interestingly, MCR type III lacks the methyl-cysteine but possesses in subunit α of M. formicicus a 6-hydroxy-tryptophan, which thus far has been found only in the α-amanitin toxin peptide but not in proteins. IMPORTANCE Methyl coenzyme M reductase (MCR) represents a prime target for the mitigation of methane releases. Phylogenetic analyses of MCRs suggested several distinct sequence clusters; those from Methanobacteriales and Methanococcales were subdivided into three types: MCR type I from Methanobacteriales, MCR type II from Methanobacteriales and Methanococcales, and the newly designated MCR type III exclusively from Methanococcales. We determined the first X-ray structures for an MCR type III. Detailed analyses revealed substantial differences between the three types only in the peripheral region. The subtle modifications identified and electrostatic profiles suggested enhanced substrate binding for MCR type III. In addition, MCR type III from Methanotorris formicicus contains 6-hydroxy-tryptophan, a new posttranslational modification that thus far has been found only in the α-amanitin toxin.

scholarly journals Molecular Evolution of a Developmental Pathway: Phylogenetic Analyses of Transforming Growth Factor-β Family Ligands, Receptors and Smad Signal Transducers

Genetics ◽  
1999 ◽  
Vol 152 (2) ◽  
pp. 783-795 ◽  
Author(s):  
Stuart J Newfeld ◽  
Robert G Wisotzkey ◽  
Sudhir Kumar
Keyword(s):  
Growth Factor ◽  
Transforming Growth Factor ◽  
Genomic Sequence ◽  
Phylogenetic Analyses ◽  
Transforming Growth Factor Β ◽  
Type I ◽  
Type Ii ◽  
Intercellular Signaling ◽  
Signal Transducers ◽  
Transitional State

Abstract Intercellular signaling by transforming growth factor-β (TGF-β) proteins coordinates developmental decisions in many organisms. A receptor complex and Smad signal transducers are required for proper responses to TGF-β signals. We have taken a phylogenetic approach to understanding the developmental evolutionary history of TGF-β signaling pathways. We were interested in detecting evolutionary influences among the physically interacting multigene families encoding TGF-β ligands, receptors, and Smads. Our analyses included new ligands and Smads identified from genomic sequence as well as the newest published family members. From an evolutionary perspective we find that (1) TGF-β pathways do not predate the divergence of animals, plants, and fungi; (2) ligands of the TGF-β/activin subfamily likely originated after the divergence of nematodes and arthropods; (3) type I receptors from Caenorhabditis elegans are distinct from other receptors and may reflect an ancestral transitional state between type I and type II receptors; and (4) the Smad family appears to be evolving faster than, and independently of, ligands and receptors. From a developmental perspective we find (1) numerous phylogenetic associations not previously detected in each multigene family; (2) that there are unidentified pathway components that discriminate between type I and type II receptors; (3) that there are more Smads to be discovered in Drosophila and mammals; and (4) that the number of C-terminal serines is the best predictor of a Smad’s role in TGF-β signal transduction. We discuss these findings with respect to the coevolution of physically interacting genes.

scholarly journals The Potential to Infer the Historical Pattern of Cultural Macroevolution

2020 ◽  
Author(s):  
Dieter Lukas ◽  
Mary Towner ◽  
Monique Borgerhoff Mulder
Keyword(s):  
Phylogenetic Analyses ◽  
Rate Of Change ◽  
Human Populations ◽  
Type I ◽  
Simulation Tool ◽  
Type Ii ◽  
Phylogenetic Methods ◽  
History Of ◽  
Potential Impact ◽  
Type Ii Errors

Phylogenetic analyses increasingly take centre-stage in our understanding of the processes shaping patterns of cultural diversity and cultural evolution over time. Just as biologists explain the origins and maintenance of trait differences among organisms using phylogenetic methods, so anthropologists studying cultural macroevolutionary processes use phylogenetic methods to uncover the history of human populations and the dynamics of culturally transmitted traits. In this paper we revisit concerns with the validity of these methods. Specifically, we use simulations to reveal how properties of the sample (size, missing data), properties of the tree (shape), and properties of the traits (rate of change, number of variants, transmission mode) might influence the inferences that can be drawn about trait distributions across a given phylogeny and the power to discern alternative histories. Our approach shows that in two example datasets specific combinations of properties of the sample, of the tree, and of the trait can lead to potentially high rates of Type I and Type II errors. We offer this simulation tool to help assess the potential impact of this list of persistent perils in future cultural macroevolutionary work.

scholarly journals SARS-CoV-2 Evolutionary Adaptation toward Host Entry and Recognition of Receptor O-Acetyl Sialylation in Virus–Host Interaction

2020 ◽  
Vol 21 (12) ◽  
pp. 4549 ◽  
Author(s):  
Cheorl-Ho Kim
Keyword(s):  
Gene Transfer ◽  
Specific Interaction ◽  
Virus Evolution ◽  
Influenza Viruses ◽  
Host Cells ◽  
Type I ◽  
Evolutionary Adaptation ◽  
Type Ii ◽  
Health Crisis ◽  
Host Tropism

The recently emerged SARS-CoV-2 is the cause of the global health crisis of the coronavirus disease 2019 (COVID-19) pandemic. No evidence is yet available for CoV infection into hosts upon zoonotic disease outbreak, although the CoV epidemy resembles influenza viruses, which use sialic acid (SA). Currently, information on SARS-CoV-2 and its receptors is limited. O-acetylated SAs interact with the lectin-like spike glycoprotein of SARS CoV-2 for the initial attachment of viruses to enter into the host cells. SARS-CoV-2 hemagglutinin-esterase (HE) acts as the classical glycan-binding lectin and receptor-degrading enzyme. Most β-CoVs recognize 9-O-acetyl-SAs but switched to recognizing the 4-O-acetyl-SA form during evolution of CoVs. Type I HE is specific for the 9-O-Ac-SAs and type II HE is specific for 4-O-Ac-SAs. The SA-binding shift proceeds through quasi-synchronous adaptations of the SA-recognition sites of the lectin and esterase domains. The molecular switching of HE acquisition of 4-O-acetyl binding from 9-O-acetyl SA binding is caused by protein–carbohydrate interaction (PCI) or lectin–carbohydrate interaction (LCI). The HE gene was transmitted to a β-CoV lineage A progenitor by horizontal gene transfer from a 9-O-Ac-SA–specific HEF, as in influenza virus C/D. HE acquisition, and expansion takes place by cross-species transmission over HE evolution. This reflects viral evolutionary adaptation to host SA-containing glycans. Therefore, CoV HE receptor switching precedes virus evolution driven by the SA-glycan diversity of the hosts. The PCI or LCI stereochemistry potentiates the SA–ligand switch by a simple conformational shift of the lectin and esterase domains. Therefore, examination of new emerging viruses can lead to better understanding of virus evolution toward transitional host tropism. A clear example of HE gene transfer is found in the BCoV HE, which prefers 7,9-di-O-Ac-SAs, which is also known to be a target of the bovine torovirus HE. A more exciting case of such a switching event occurs in the murine CoVs, with the example of the β-CoV lineage A type binding with two different subtypes of the typical 9-O-Ac-SA (type I) and the exclusive 4-O-Ac-SA (type II) attachment factors. The protein structure data for type II HE also imply the virus switching to binding 4-O acetyl SA from 9-O acetyl SA. Principles of the protein–glycan interaction and PCI stereochemistry potentiate the SA–ligand switch via simple conformational shifts of the lectin and esterase domains. Thus, our understanding of natural adaptation can be specified to how carbohydrate/glycan-recognizing proteins/molecules contribute to virus evolution toward host tropism. Under the current circumstances where reliable antiviral therapeutics or vaccination tools are lacking, several trials are underway to examine viral agents. As expected, structural and non-structural proteins of SARS-CoV-2 are currently being targeted for viral therapeutic designation and development. However, the modern global society needs SARS-CoV-2 preventive and therapeutic drugs for infected patients. In this review, the structure and sialobiology of SARS-CoV-2 are discussed in order to encourage and activate public research on glycan-specific interaction-based drug creation in the near future.

scholarly journals Toxin Inactivation in Toxin/Antitoxin Systems

2019 ◽  
Author(s):  
Laura Fernandez-Garcia ◽  
Jun-Seob Kim ◽  
Maria Tomas ◽  
Thomas K. Wood
Keyword(s):  
Gene Transfer ◽  
Horizontal Gene Transfer ◽  
Metabolic Activity ◽  
Type I ◽  
Type Ii ◽  
Genetic Elements ◽  
Type V ◽  
Chromosomal Mutations

Toxin/antitoxin (TA) systems are used primarily to inhibit phage, reduce metabolic activity during stress, and maintain genetic elements. Given the extreme toxicity of some of the toxins of these TA systems, we were curious how the cell silences toxins, if the antitoxin is inactivated or when toxins are obtained without antitoxins via horizontal gene transfer. Here we find that the RalR (type I), MqsR (type II), GhoT (type V), and Hha (type VII) toxins are inactivated primarily by a mutation that inactivates the toxin promoter or via the chromosomal mutations iraM and mhpR.

scholarly journals Inhibition of interleukin-1 responsiveness by type II receptor gene transfer: a surface "receptor" with anti-interleukin-1 function.

1996 ◽  
Vol 183 (4) ◽  
pp. 1841-1850 ◽  
Author(s):  
F Re ◽  
M Sironi ◽  
M Muzio ◽  
C Matteucci ◽  
M Introna ◽  
...  
Keyword(s):  
Gene Transfer ◽  
Deletion Mutant ◽  
Receptor Gene ◽  
Interleukin 1 ◽  
Signal Transduction Pathway ◽  
Surface Expression ◽  
Cytokine Gene Expression ◽  
Type I ◽  
Type Ii ◽  
Transfected Cells

The hypothesis that the type II receptor (RII) acts as a decoy for interleukin-1 (IL-1) was tested by gene transfer in cells expressing only the type I receptor (8387 fibroblasts). RII-transfected cells showed defective responsiveness to IL-1 in terms of NFkappaB activation, cytokine gene expression and production. Blocking monoclonal antibodies against RII restored the capacity of RII-transfected cells to respond to IL-1 beta. Hence defective IL-1 responsiveness of RII-transfected cells requires surface expression of the molecule. RII-transfected cells showed normal responsiveness to TNF, which shares functional properties and elements in the signal transduction pathway with IL-1. Cells transfected with a deletion mutant of RII missing 26 of 29 amino acids of the cytoplasmic portion of the molecule showed impaired responsiveness to IL-2. Cells transfected with full-length or the cytoplasmic deletion mutant of RII released copious amounts of RII in the supernatant. However, transfected cells showed defective responsiveness to brief exposure to IL-1, in the absence of measurable released RII. These results indicate that impairment of the responsiveness to IL-1 following RII gene transfer was dependent upon surface expression of the molecule, specific for IL-1 and unaffected by truncation of the cytoplasmic portion. Thus, the type II "receptor" is a decoy surface molecule, regulated by antiinflammatory signals, whose only known function is to capture and block IL-1.

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