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Adhesive bond of veneering composites on various metal surfaces using silicoating, titanium-coating or functional monomers.

OBJECTIVES: This study compared the shear bond strength (SBS) between veneering composites and titanium (grade 1), a cobalt-chromium-alloy and a high precious-alloy, which were pretreated using silicoating systems, functional monomers or an experimental titanium-dioxide coating system. METHOD: The specimens were sized to rectangular plates of 20 x10 x 2mm(3) (l,w,h) and a composite cylinder (height of 4mm, diameter 5mm) was axially polymerized to the middle of the plates. After aging (24h or 150 d storage in distilled water at 37 degrees C, or thermal-cycling: 6000 x 5 degrees /55 degrees C) the SBS was determined. RESULTS: Independent of the type of metal and the conditioning/coating techniques the lowest SBSs were found after thermal-cycling. Titanium. The SBS of the silica coating systems and the functional monomers did not differ statistically on titanium. However, the titanium-dioxide coating method had significantly higher values than the other methods. Cobalt-chromium. The highest mean values were observed with the titanium-dioxide coating system and the phosphate acid ester. Precious alloy. No statistical significant different SBS was found for the silicoating and the titanium-dioxide coating methods, while the functional monomers were statistically significant (lower) different to both systems. CONCLUSION: Generally, the titanium-dioxide coating system achieved the highest SBS under different aging conditions and on all three different metal-surfaces.

Adhesives↗

[In silico cloning of glucose-6-phosphate dehydrogenase cDNA from rice (Oryza sativa L.)].

In silico cloning was a new strategy of gene cloning developed with the development of genome, EST projects and bioinformatics. Using wheat glucose-6-phosphate dehydrogenase cDNA (clone: Tagpdl) sequence as a querying probe, one highly homologous BAC clone sequence was obtained from rice sequence database of GenBank and the putative cDNA sequence of rice glucose-6-phosphate dehydrogenase was assembled according to the wheat clone. Furthermore, the full-length cDNA of rice glucose-6-phosphate dehydrogenase was cloned by RT-PCR with two primers designed based on this assembled cDNA sequence. Since this fragment contained a complete ORF of 1515 bp with a stop codon in its upstream and poly(A) signal in its downstream, it could be concluded that a full-length gene (GenBank accession number AY078072), which was named as OsG6PDH. Homology analysis of OsG6PDH showed a 88% identity with wheat and the deduced amino acid showed 89%, 79% and 80% homology with G6PDH from wheat, tomato and tobacco respectively. OsG6PDH was expressed in inflorescence, embryo, root and leaf of rice, with a slightly higher in inflorescence and root. It was also discussed in this paper that the application of in silico cloning in the isolation of functional genes from rice.

Base Sequence↗

Effect of diatomaceous earths Fossil Shield and Silico-Sec on the egg laying behaviour of Callosobruchus maculatus (F.) (Coleoptera: Bruchidae).

The pulse beetle, Callosobruchus maculatus (F.) is a destructive pest of pulses in both storage and field. It is well known that diatomaceous earth (DE) kill the insects by locally absorbing the epicuticular lipid layers leading to high rate of water loss through the cuticle. However, the effectiveness of DE depends on its ability to kill the adults before copulation and egg-laying. Newly emerged virgin males and females of Callosobruchus maculatus (F.) were exposed to the DEs, Fossil-Shield and Silico-Sec on 30 treated mungbeans (Vigna radita (L)). Fecundity, number of beans used for egg-laying and beans without eggs were evaluated after four days; the number of unhatched eggs was evaluated after ten days. It was determined, that the fecundity of female insects decreased sigmoidely with increasing rate of DE content. Percentages of unhatched eggs and seeds without eggs increased with increasing DE dosages. However, the maximum egg densities (eggs per used secd) occurred at 1200 mg DE/kg for Fossil-Shield and Silico-Sec. The reason for such DE-stimulated behaviour of egg laying expressed as a number of seeds with eggs of C. maculatus is not known, but it may be related to the stress caused by the inert dusts or to the reduction of both chemical and physical (tactile) stimuli. Treatment with DEs altered the surface texture of the beans and caused less cohesion between eggs and the seed surface. Only few larvae managed to penetrate into the grains, possibly due to increased grain roughness and repellent effect of DE. A relatively high number of eggs were laid on the surface of those beans where the amount of dust had been locally reduced by adults' movement and their pick up of DE. Therefore, several larvae tried to penetrate into these treated beans, causing a high larval density per partially cleaned bean. All these reasons lead to a progeny decline.

Animals↗

Proteomic informatics: in silico methods lead to data management challenges.

Proteomics, which identifies proteins and analyzes their function in cells, is foreseen as the next challenge in biomedicine as diseases in the body are most easily recognized through the function of their proteins. Achieving this recognition is more difficult than pure gene analysis: it is estimated that 35,000 genes are present in human DNA, encoding more than 1 million proteins. A myriad of in vitro and in silico technologies now exist for studying proteins and their biological function. This review focuses on the vast array of in silico proteomic analysis methods, highlights public and commercial repositories for this data, and discusses the challenges associated with resolving and integrating the knowledge originating from this data.

Amino Acid Sequence↗

[Study on drug-resistance of Mycobacterium tuberculosis isolated from coal workers with silico-tuberculosis].

OBJECTIVE: To study the gene mutation and streptomycin, isoniazid or rifampicin resistance of Mycobacterium isolated from silico-tuberculosis patient's sputum so as to find a more effective therapy for this disease. METHODS: Mycobacteria tuberculosis were separated from 96 coal worker with silico-tuberculosis firstly. Then rpsL, KatG and rpoB fragments of genome were copied with PCR and compared their SSCP profiles with standard strains. RESULTS: 67 strains of streptomycin, isoniazid or rifampicin resistant Mycobacteria tuberculosis were found in routine drug resistance test, with the percentages of 80.5% (54/67), 58.2% (39/67) respectively. PCR-SSCP showed that out of 67 drug-resistant strains, 66(98.5%) of rpsL, 47(70.1%) of rpoB and 42(62.7%) of KatG appeared abnormal. CONCLUSION: Most of the resistant strains appeared gene mutation. The mution rates were higher than the results from routine drug resistance test.

Coal↗

Trophoblastic cDNA cloning of porcine Pregnancy-Associated Glycoprotein genes (pPAG) and in silico analysis of coded polypeptide precursors.

Multiple Pregnancy-Associated Glycoprotein (PAG) genes, coding various chorionic products that belong to the aspartic proteinase family (AP), have been discovered in various eutherians (Placentalia). This paper presents cloning of five novel porcine PAG (pPAG) cDNAs: pPAG3, pPAG4, pPAG5, pPAG6, pPAG8 and pPAG10. All cDNAs have been identified by trophoblastic library screening on 13-17 days post coitum (dpc). These cloned and sequenced pPAG cDNAs have been deposited in GenBank database of National Institute of Heath/ National Center of Biotechnology Information (NIH/NCBI) with various accession numbers: AF315377, AF272734, AY188554, AF272735, AY373029 and one during submission. The open reading frames (ORF) of cloned cDNA sequences allowed for identification and in silico analysis of polypeptide pPAG precursors, including their identity content and various amino acid substitutions, which caused hypothetical structure changes of the pPAG precursors. In conclusion, our results concerning transcriptomal cloning and in silico analyses of the novel identified trophoblastic cDNA of the pPAG genes provided contributive data regarding porcine genome identification and physiology of the gestation in this species.

Amino Acid Sequence↗

[Analysis, identification and correction of some errors of model refseqs appeared in NCBI Human Gene Database by in silico cloning and experimental verification of novel human genes].

We found that human genome coding regions annotated by computers have different kinds of many errors in public domain through homologous BLAST of our cloned genes in non-redundant (nr) database, including insertions, deletions or mutations of one base pair or a segment in sequences at the cDNA level, or different permutation and combination of these errors. Basically, we use the three means for validating and identifying some errors of the model genes appeared in NCBI GENOME ANNOTATION PROJECT REFSEQS: (I) Evaluating the support degree of human EST clustering and draft human genome BLAST. (2) Preparation of chromosomal mapping of our verified genes and analysis of genomic organization of the genes. All of the exon/intron boundaries should be consistent with the GT/AG rule, and consensuses surrounding the splice boundaries should be found as well. (3) Experimental verification by RT-PCR of the in silico cloning genes and further by cDNA sequencing. And then we use the three means as reference: (1) Web searching or in silico cloning of the genes of different species, especially mouse and rat homologous genes, and thus judging the gene existence by ontology. (2) By using the released genes in public domain as standard, which should be highly homologous to our verified genes, especially the released human genes appeared in NCBI GENOME ANNOTATION PROJECT REFSEQS, we try to clone each a highly homologous complete gene similar to the released genes in public domain according to the strategy we developed in this paper. If we can not get it, our verified gene may be correct and the released gene in public domain may be wrong. (3) To find more evidence, we verified our cloned genes by RT-PCR or hybrid technique. Here we list some errors we found from NCBI GENOME ANNOTATION PROJECT REFSEQs: (1) Insert a base in the ORF by mistake which causes the frame shift of the coding amino acid. In detail, abase in the ORF of a gene is a redundant insertion, which causes a reading frame shift in the translation of an alternative protein, such as LOC124919 is wrong form of C17 orf32 (with mouse and rat orthologs determined by us). (2) Put together by mistake (with force). This is a wrong assembly of non-relating cDNA segment, such as LOC147007 is wrong form of C17orf32. (3) Mistakenly insert a base or one section of cDNA in the ORF which causes it ending beforehand, only coding cDNA sequence of N-terminal amino acids, incomplete. For example, LOC123722 is wrong form of SPRYD1, and even the human hypothetical gene LOC126250 or PDCD5 is wrong form of our PDCD5 (TFAR19). (4) Incomplete, only coding cDNA sequence of C-terminal amino acids. For example, human LOC149076 and mouse LOC230761 are wrong form of our verified human ZNF362 and mouse Zfp362, respectively. (5) Incomplete, only coding one section of coding protein cDNA sequence of correct gene ORF, lacking N-terminal and C-terminal amino acids sequence, and at the same time, mistakenly anticipates the first non-initiation codon amino acid of the incomplete protein amino acid as the initiation codon, e.g. anticipating L as M. For example, LOC200084 is wrong form of ZNF362. (6) Mistakenly insert a base or one section of cDNA in the ORF, wrongly causing unwanted termination codon before the insertion, so the coding protein lacks the first part of the amino acids. For example, the GenBank Acc. No. AL096883 ( LOCUS No. HS323M22B) is wrong form of an experimentally verified human NM_012263 with mouse ortholog of BC010510 determined. (7) It may regard the polluted genomic sequence as complete gene cDNA sequence and anticipate the so-called single exon gene, even the real one, only a small ORF in the very long single exon mRNA, while there really exists termination code in the same phase of the upper part of the ORF initiation code, no other characters accord with the gene's condition. For example, LOC91126 is wrong form of ZNF362. (8) The anticipated genes only have ORF which has no EST proofs on both terminal sides. Depending on this ORF, a complete gene cDNA with double support of EST and human genome (there are termination codes at the same phase of the upper part of ORF) which indicates the anticipated ORF reference sequence may be incorrect. For example, LOC164395 may be wrong form of novel human gene bankit4590055. (9) A similar but smaller protein-coding gene is anticipated in the range of the human genome sequence that has the support of EST experimental proof, so other new anticipated gene may be incorrect. For example, LOC167563 may be wrong form of CMYA5. However,these errors can be corrected or avoided by using our strategy. Here we give one example in detail: Comparision of the sequence SPRYD1 with human hypothetical gene LOC123722. The TAA bases in the position of 478-480 in LOC123722 cDNA is redundant, which causes a reading frame shift in the translation of an alternative protein. The redundancy of GTAAA of LOC123722 is not supported by our experimental clone,and is almost fully rejected by human EST alignment, and is shown as the next intron sequence by genomic GT/AG organization analysis. The verification of cDNA or genomic DNA sequence of SPRYD1 implies that LOC123722 has a wrong stop codon within its ORF because of the prediction program, thus being not complete cds. To sum up, by combining bioinformatics analyses with experimental verification, we have found that there are many errors of at least nine kinds appeared in NCBI GENOME ANNOTATION PROJECT REFSEQs through BLAST of our cloned genes in non-redundant database, and our strategy is helpful in correcting them, such as LOC14907, LOC200084 and LOC91126 (all of them should be ZNF362, but are three different kinds of wrong forms of ZNF362), three model reference sequences predicted from NCBI contig NT_004511 by automated computational analysis using gene prediction method, or such as LOC124919 and LOC147007 (both should be C17orf32, but are two different kinds of wrong forms of C17orf32), two model reference sequences predicted from NCBI contig NT_010808 by automated computational analysis using gene prediction method. Therefore, the correct identification and annotation of novel human genes may be still a heavy task, which can be finished within a long period of time. So human genome coding regions annotated by computer should be used with caution. The articles published in the past did not clearly point out the existence of mistakes in the NCBI human gene mode reference sequence. At the Seventh International Human Genome Conference held in April 2002, we first published the researching result on this aspect in the communication form of Posterly insert a base or one section of cDNA in the ORF, wrongly causing unwanted termination codon before the insertion, so the coding protein lacks the first part of the amino acids. For example, the GenBank Acc. No. AL096883 ( LOCUS No. HS323M22B) is wrong form of an experimentally verified human NM_012263 with mouse ortholog of BC010510 determined. (7) It may regard the polluted genomic sequence as complete gene cDNA sequence and anticipate the so-called single exon gene, even the real one, only a small ORF in the very long single exon mRNA, while there really exists termination code in the same phase of the upper part of the ORF initiation code, no other characters accord with the gene's condition. For example, LOC91126 is wrong form of ZNF362. (8) The anticipated genes only have ORF which has no EST proofs on both terminal sides. Depending on this ORF, a complete gene cDNA with double support of EST and human genome (there are termination codes at the same phase of the upper part of ORF) which indicates the anticipated ORF reference sequence may be incorrect. For example, LOC164395 may be wrong form of novel human gene bankit4590055. (9) A similar but smaller protein-coding gene is anticipated in the range of the human genome sequence that has the support of EST experimental proof, so other new anticipated gene may be incorrect. For example, LOC167563 may be wrong form of CMYA5. However, these errors can be corrected or avoided by using our strategy. Here we give one example in detail: Comparision of the sequence SPRYD1 with human hypothetical gene LOC123722. The TAA bases in the position of 478-480 in LOC123722 cDNA is redundant, which causes a reading frame shift in the translation of an alternative protein. The redundancy of GTAAA of LOC123722 is not supported by our experimental clone, and is almost fully rejected by human EST alignment, and is shown as the next intron sequence by genomic GT/AG organization analysis. The verification of cDNA or genomic DNA sequence of SPRYD1 implies that LOC123722 has a wrong stop codon within its ORF because of the prediction program, thus being not complete cds. To sum up, by combining bioinformatics analyses with experimental verification, we have found that there are many errors of at least nine kinds appeared in NCBI GENOME ANNOTATION PROJECT REFSEQs through BLAST of our cloned genes in non-redundant database, and our strategy is helpful in correcting them, such as LOC14907, LOC200084 and LOC91126 (all of them should be ZNF362, but are three different kinds of wrong forms of ZNF362), three model reference sequences predicted from NCBI contig NT_004511 by automated computational analysis using gene prediction method, or such as LOC124919 and LOC147007 (both should be C17orf32, but are two different kinds of wrong forms of C17orf32), two model reference sequences predicted from NCBI contig NT_010808 by automated computational analysis using gene prediction method. Therefore, the correct identification and annotation of novel human genes may be still a heavy task, which can be finished within a long period of time. So human genome coding regions annotated by computer should be used with caution. (ABSTRACT TRUNCATED)

Amino Acid Sequence↗

In silico predictive toxicology: the state-of-the-art and strategies to predict human health effects.

In silico predictive toxicology techniques are a fast and cost-efficient alternative or supplement to bioassays for the identification of toxic effects at an early stage of drug development. This review provides a conceptual description of the most important in silico prediction techniques and presents exemplary strategies for the prediction of human health effects. Special emphasis will be given to validation issues and the performance of models for human health-related effects.

Animals↗

Characterization of cancer stroma markers: in silico analysis of an mRNA expression database for fibroblast activation protein and endosialin.

Standardized, high-throughput RNA detection with microarray chips allows for the construction of genome-wide databases for tissue specimens suitable for in silico electronic Northern blot (eNorthern) analysis of marker genes. We used the BioExpress database, which contains transcriptional profiles of normal and cancer samples, to examine two putative markers of cancer stroma: fibroblast activation protein-alpha (FAP-alpha) and endosialin. Analyses for FAP-alpha showed that normal tissues generally lack RNA signals, with the exception of endometrium. Typing of tumors revealed prominent FAP-alpha signals in cancer types marked by desmoplasia, and localization of FAP-alpha in reactive cancer stroma was confirmed by immunohistochemistry. A subset of sarcomas displayed prominent FAP-alpha signals localizing to the malignant cells. For endosialin, eNorthern analyses showed low to moderate RNA signals in many normal organs, whereas immunohistochemistry revealed endosialin in only some tissues, such as endometrium. Endosialin was detected at the RNA and protein level in sarcomas, notably malignant fibrous histiocytomas. Low to moderate endosialin RNA signals were found in epithelial cancer types for which immunostaining identifies expression in subsets of tumor capillaries or fibroblasts. These findings extend the FAP-alpha and endosialin profiling in silico to an unbiased tumor database and place both molecules in a novel context of endometrial biology and sarcoma subtyping. Our findings suggest that BioExpress can be searched directly for tumor stroma markers but may need prior enrichment for markers with narrow cellular representation, such as endosialin. Constructing databases from microdissected cancer tissues may be an essential step for tumor stroma-targeted therapies.

Adult↗

[Power estimation for in silico mapping].

A fundamentally new approach to gene mapping of complex traits was suggested recently. It consists in computer analysis of existing databases on the phenotypes and single nucleotide polymorphisms (SNPs) in inbred mouse strains and was termed in silico mapping. The power of this method has been studied by simulating quantitative traits controlled by one, two, or three genes. The results have demonstrated that the power of in silico mapping is high in the case of a monogenic trait. The probability of mapping all genes determining a digenic or, especially, trigenic trait is low. If two or three genes make equal phenotypic contributions to a trait, the proportions of experiments where none of them is localized are 17 and 25%, respectively. In the case of a major gene effect, when the phenotypic contribution of one gene considerably exceeds those of the other genes, the probability to map the major gene is 0.95 and 0.80 for the digenic and trigenic models, respectively. This shows that, in the case of polygenic control, the new method could localize only the genes with major effects, while most genes involved in the control of the trait would not be mapped.

Animals↗

In silico analysis of Burkholderia pseudomallei genome sequence for potential drug targets.

Recent advances in DNA sequencing technology have enabled elucidation of whole genome information from a plethora of organisms. In parallel with this technology, various bioinformatics tools have driven the comparative analysis of the genome sequences between species and within isolates. While drawing meaningful conclusions from a large amount of raw material, computer-aided identification of suitable targets for further experimental analysis and characterization, has also led to the prediction of non-human homologous essential genes in bacteria as promising candidates for novel drug discovery. Here, we present a comparative genomic analysis to identify essential genes in Burkholderia pseudomallei. Our in silico prediction has identified 312 essential genes which could also be potential drug candidates. These genes encode essential proteins to support the survival of B. pseudomallei including outer-inner membrane and surface structures, regulators, proteins involved in pathogenenicity, adaptation, chaperones as well as degradation of small and macromolecules, energy metabolism, information transfer, central/intermediate/miscellaneous metabolism pathways and some conserved hypothetical proteins of unknown function. Therefore, our in silico approach has enabled rapid screening and identification of potential drug targets for further characterization in the laboratory.

Burkholderia pseudomallei↗

[Effect of sandblast treatment on resin-alloys bond strength by silicoating technique].

The purpose of this study was to investigate why sandblast treatment increases the bond strength of resin-alloy by the Silicoating technique. In this study, two types of alloy specimens, namely Ag-Pd alloy and Ni-Cr alloy, were prepared by casting. These specimens were given sandblast treatment by 37 microns or 250 microns Al2O3 particle under the following conditions: 3 kg/cm2 for 30 sec, 5 kg/cm2 for 10 sec, 30 sec and 45 sec, and 7 kg/cm2 for 30 sec. Under each condition of sandblast treatment, changes in roughness and wettability of the alloy surface were measured. After this treatment, the alloy surface was Silicoated, and then a light-cured resin was bonded to it. Specimens were stored in air for one week and thermal cycled from 4 to 60 degrees C for 10(4) cycles. The bond strength was measured by compressive shear stress. It was shown that the sandblast treatment caused the surface area to increase in the range of 1.3-1.9 times. Also, the sandblast treatment made the alloy-water contact angle smaller and wettability greater. Maximum bond strengths for Ag-Pd alloy and Ni-Cr alloy, when sandblast treated and stored in the air for one week, were 213.7 kg/cm2 and 198.7 kg/cm2 respectively. On the other hand, bond strengths for Ag-Pd alloy and Ni-Cr alloy after thermal cycling were 129.5 kg/cm2 and 159.9 kg/cm2 respectively. These values of bond strength were 2-3 times greater than those of for specimens not given the sandblast treatment. However, varying the conditions of sandblast treatment did not produce any significant differences.

Chromium Alloys↗

Tensile strength and microleakage of the bond between a nickel-chromium alloy and a visible light-cured resin composite: effect of 4-META, silicoating, and bead retention.

Three retention systems, 4-META adhesive, Silicoating, and a conventional retention beads system, were used for resin-metal bonding. For each group, 40 standard specimens were prepared (20 for microleakage testing and 20 for tensile strength testing). Wax patterns were prepared, invested, and cast with a nickel-chromium alloy. The metal surfaces of the specimens were sandblasted with 250-microns aluminum oxide. Dentacolor Opaque was placed and set in a light curing unit for 90 seconds. Dentacolor resin composite was placed and set in the same unit for 90 seconds. The bonded specimens were subjected to thermocycling process in baths of 5 degrees C and 55 degrees C with 30-second dwell time. The tensile strength test specimens were stored in water, and the microleakage test specimens were stored in 5% basic fuchsin dye for 2 days. The means of the tensile strength test groups were not significantly different. However, the differences in microleakage among groups were found to be statistically significant. As a result, 4-META and Silicoating systems were found to be better than the conventional retention beads system, which allowed the greatest microleakage.

Chromium Alloys↗

In silico profiling of tyrosine kinases binding specificity and drug resistance using Monte Carlo simulations with the ensembles of protein kinase crystal structures.

The molecular basis of the tyrosine kinases binding specificity and drug resistance against cancer drugs Imatinib and Dasatinib is elucidated using Monte Carlo simulations of the inhibitor-receptor binding with the ensembles of protein kinase crystal structures. In silico proteomics analysis unravels mechanisms by which structural plasticity of the tyrosine kinases is linked with the conformational preferences of Imatinib and Dasatinib in achieving effective drug binding with a distinct spectrum of the tyrosine kinome. The differences in the inhibitor sensitivities to the ABL kinase mutants are rationalized based on variations in the binding free energy profiles with the conformational states of the ABL kinase. While Imatinib binding is highly sensitive to the activation state of the enzyme, the computed binding profile of Dasatinib is remarkably tolerant to the conformational state of ABL. A comparative analysis of the inhibitor binding profiles with the clinically important ABL kinase mutants has revealed an excellent agreement with the biochemical and proteomics data. We have found that conformational adaptability of the kinase inhibitors to structurally different conformational states of the tyrosine kinases may have pharmacological relevance in acquiring a specific array of potent activities and regulating a scope of the inhibitor resistance mutations. This study outlines a useful approach for understanding and predicting the molecular basis of the inhibitor sensitivity against potential kinase targets and drug resistance.

Computational Biology↗

A functional genomics approach using metabolomics and in silico pathway analysis.

In the field of functional genomics increasing effort is being undertaken to analyze the function of orphan genes using metabolome data. Improved analytical equipment allows screening simultaneously for a high number of metabolites. Such metabolite profiles are analyzed using multivariate data analysis techniques and changes in the genotype will in many cases lead to different metabolite profiles. Here, a theoretical framework that may be applied to identify the function of orphan genes is presented. The approach is based on a combination of metabolome analysis combined with in silico pathway analysis. Pathway analysis may be carried out using convex analysis and a change in the active pathway structure of deletion mutants expressed in a different metabolite profile may disclose the function or the functional class of an orphan gene. The concept is illustrated using a simplified model for growth of Saccharomyces cerevisiae.

Algorithms↗

In silico prediction and validation of the importance of the Entner-Doudoroff pathway in poly(3-hydroxybutyrate) production by metabolically engineered Escherichia coli.

The metabolic network of Escherichia coli was constructed and was used to simulate the distribution of metabolic fluxes in wild-type E. coli and recombinant E. coli producing poly(3-hydroxybutyrate) [P(3HB)]. The flux of acetyl-CoA into the tricarboxylic acid (TCA) cycle, which competes with the P(3HB) biosynthesis pathway, decreased significantly during P(3HB) production. It was notable to find from in silico analysis that the Entner-Doudoroff (ED) pathway flux increased significantly under P(3HB)-accumulating conditions. To prove the role of ED pathway on P(3HB) production, a mutant E. coli strain, KEDA, which is defective in the activity of 2-keto-3-deoxy-6-phosphogluconate aldolase (Eda), was examined as a host strain for the production of P(3HB) by transforming it with pJC4, a plasmid containing the Alcaligenes latus P(3HB) biosynthesis operon. The P(3HB) content obtained with KEDA (pJC4) was lower than that obtained with its parent strain KS272 (pJC4). The reduced P(3HB) biosynthetic capacity of KEDA (pJC4) could be restored by the co-expression of the E. coli eda gene, which proves the important role of ED pathway on P(3HB) synthesis in recombinant E. coli as predicted by metabolic flux analysis.

Alcaligenes↗

In silico genome-scale reconstruction and validation of the Staphylococcus aureus metabolic network.

A genome-scale metabolic model of the Gram-positive, facultative anaerobic opportunistic pathogen Staphylococcus aureus N315 was constructed based on current genomic data, literature, and physiological information. The model comprises 774 metabolic processes representing approximately 23% of all protein-coding regions. The model was extensively validated against experimental observations and it correctly predicted main physiological properties of the wild-type strain, such as aerobic and anaerobic respiration and fermentation. Due to the frequent involvement of S. aureus in hospital-acquired bacterial infections combined with its increasing antibiotic resistance, we also investigated the clinically relevant phenotype of small colony variants and found that the model predictions agreed with recent findings of proteome analyses. This indicates that the model is useful in assisting future experiments to elucidate the interrelationship of bacterial metabolism and resistance. To help directing future studies for novel chemotherapeutic targets, we conducted a large-scale in silico gene deletion study that identified 158 essential intracellular reactions. A more detailed analysis showed that the biosynthesis of glycans and lipids is rather rigid with respect to circumventing gene deletions, which should make these areas particularly interesting for antibiotic development. The combination of this stoichiometric model with transcriptomic and proteomic data should allow a new quality in the analysis of clinically relevant organisms and a more rationalized system-level search for novel drug targets.

Computational Biology↗

An in silico model for HIF-alpha regulation and hypoxia response in tumor cells.

The dependency of the growth and metastasis of tumors on the new blood vessel formation, or angiogenesis, has opened up new potentials to tumor therapy, nevertheless understanding the molecular mechanisms involved in angiogenesis is crucial in the bioengineering of novel anti-angiogenic drugs. The key component in hypoxia sensing in tumor cells is the hypoxia-inducible factor, HIF-1alpha, which is inactivated through proteosome-mediated degradation under normoxic conditions. Two enzymes have been reported to hydroxylate HIF-1alpha, namely prolyl hydroxylase (PH), recruiting the proetasome complex and degrading cytoplasmic HIF-1alpha, and asparaginyl hydroxylase/factor inhibiting HIF-1alpha (FIH-1), downregulating the recruitment of p300 to the promoter, thereby reducing the transcriptional activity of HIF-1alpha. In this study, we have constructed an in silico model of a tumor cell using the GEPASI 3.30 biochemical simulation software (http://www.gepasi.org) and studied the performances of PH and FIH-1 on HIF-1alpha degradation and inactivation, respectively, as monitored by expression of the vascular endothelial growth factor, VEGF, during hypoxia. In our biochemical models, FIH-1 can successfully increase hypoxic transcription of VEGF, however FIH-1 on its own is not sufficient to inactivate HIF-1 completely, leading to background VEGF transcription under normoxic conditions. On the other hand, PH is necessary to increase the hypoxic transcriptional response, and can effectively shut off normoxic transcription. We therefore propose that regulating PH activity can be a primary target for anti-angiogenic bioengineering research.

Computational Biology↗