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PubMed2002

Distribution of p53 codon 72 polymorphism in Indian primary open angle glaucoma patients.

PURPOSE: Glaucoma is a complex neurodegenerative disorder of the eye. Primary Open Angle Glaucoma (POAG) is the most common type, accounting for over half of the total cases. Recently, a significant difference in the distribution of the codon 72 polymorphism of the tumor suppressor gene p53 between control subjects and POAG patients of Chinese origin (p=0.00782) was demonstrated. The proline residue at codon 72 of the p53 gene was significantly over represented in the POAG patients relative to healthy controls. The purpose of this study was to investigate whether the reported association between the p53 polymorphism and POAG is a common phenomenon irrespective of geographical location or ethnicity of the population. METHODS: Sixty seven unrelated POAG patients, ranging from 10-65 years of age (mean+/-SD of 41.16+/-18.52 years), and 112 control subjects having a similar age range of 18-63 years (mean+/-SD of 36.64+/-14.65 years) were enrolled in this study. A region of the p53 gene encompassing two polymorphic sites, a 16 bp duplication in intron 3 and a BstU I RFLP in exon 4, were amplified by polymerase chain reaction from Indian POAG patients and normal healthy controls. A single base change (G to C) in codon 72 alters the amino acid residue from arginine to proline and removes the polymorphic BstU I site mentioned above. The amplified DNA fragments were digested with the restriction enzyme and the digestion patterns of the fragments were used to identify the alleles for both the polymorphic sites. RESULTS: No significant association between p53 alleles and Indian POAG patients were observed by analyzing either codon 72 polymorphism (p=0.5627) or the intronic 16 bp duplication polymorphism (p=0.059). Haplotype analysis, reported to be a better predictor of association of the p53 gene with different types of cancer, was also performed and no association of any haplotype was detected with POAG (p=0.1831). CONCLUSIONS: Association between the p53 gene encoding for proline at codon 72 and POAG presumably exists in some ethnic populations but cannot be used as a predictor for the role of the gene as a common regulator of cell death of retinal ganglions leading to POAG.

Adolescent↗
PubMed2003

Codon usage-mediated inhibition of HIV-1 gag expression in mammalian cells occurs independently of translation.

Codon usage is considered one of the critical factors that limit the expression rate of heterologous genes. Impaired translation efficiency, specifically insufficient amount of corresponding tRNAs and changed startcodon context, are believed to account for the low translation initiation and elongation rates during the protein biosynthesis in unicellular organisms. Translational efficiency is probably not the primary factor influencing codon usage diversity in mammalian cells. However, the other possible mechanisms preventing expression of genes with low-usage such as mRNA stability, processing and nucleocytoplasmic transport, are not adequately explored. In our work, we addressed the question of whether codon usage differences affect exclusively translational efficiency of mammalian gene products. We demonstrated that the CMV-induced expression of gag-reporter in human H1299 cell line was influenced by the nucleotide composition of the mRNA, and the limitation of gag expression appeared to be inversely related to the level of codon optimization. However, cytoplasmic expression of the gag-reporter driven by vaccinia virus/T7 RNA polymerase hybrid system rescued its expression independently of HIV-1 gag mRNA nucleotide content. We concluded that impaired HIV-1 gag expression may be caused by translation-independent mechanisms, which probably play a major role in codon usage-mediated defects in heterologous gene expression in mammalian cells.

Codon↗
PubMed2003

Age-associated increase of codon 72 Arginine p53 frequency in gastric cardia and non-cardia adenocarcinoma.

PURPOSE: A common polymorphism of the tumor suppressor gene TP53 at codon 72 has been associated with human cancer susceptibility and prognosis. To examine the role of the polymorphism in the gastric adenocarcinoma, we examined 397 patients with or without the cancer. EXPERIMENTAL DESIGN: DNA samples were extracted from archived gastric tumor tissues and/or normal tissues of gastric adenocarcinoma and noncancer patients. The TP53 codon 72 genotypes were determined by PCR-RFLP. RESULTS: The overall genotype frequencies for Pro/Pro, Arg/Pro, and Arg/Arg were 7.3, 45.1, and 47.6%, respectively. A significant stepwise increased frequency of codon 72 Arg p53 with age was observed in patients with gastric cancer, but not in noncancer patients (P = 0.01). Patients with gastric cardia cancer had a significantly higher frequency of homozygous Arg allele than those with non-cardia tumors (P = 0.03) or than noncancer patients. After adjustment for age and gender, a logistic regression analysis suggested that the risk for a p53 Arg homozygous patient to develop cardia cancer is 3.1 95% confidence interval, 1.4-7.3) times greater than for p53 Pro homozygous and p53 Arg/Pro heterozygous patients. No close relationship was observed among patient gender, tumor histological type, p53 protein expression, and codon 72 genotype distribution. CONCLUSIONS: These findings indicate that codon 72 Arg p53 may be associated with a prolonged survival for patients who have had gastric adenocarcinoma, especially non-cardia adenocarcinoma. It may confer, however, a different role on patients who suffer cardia gastric adenocarcinoma.

Adenocarcinoma↗
PubMedDate not supplied

[Highly conserved region 1816-1831 of the 18S ribosomal RNA is close to the first nucleotide of the A-site codon in elongation and termination of translation].

Two mRNA analogs, pUUCUAAA (with stop codon UAA) and pUUCUCAA (with Ser codon UCA) containing a perfluoroarylazido group at U4, were used to study the position relative to the 18S rRNA for the first nucleotide of the codon located in the A site of the human 80S ribosome. To place UAA or UCA in the A site, UCC-recognizing tRNAPhe was bound in the P site. With each analog, crosslinking was detected for highly conserved fragment 1816-1831, which contains invariant dinucleotide A1823/A1824 and is in helix 44 at the 3' end of the 18S rRNA. Since 18S rRNA modification did not depend on whether the U4 photoreactive group was in the sense or stop codon, it was assumed that polypeptide chain release factor 1 directly recognizes the trinucleotide of a stop codon located in the A site.

Base Sequence↗
PubMedDate not supplied

[Rare codons and gene expression in Escherichia coli].

Influence of rare codons upon gene expression in E. coli was investigated. The chimeric gene was created combining CAT gene and a fragment of the gene, encoding for alpha-domain of beta-galactosidase. The synthetic oligonucleotides were inserted in different parts of the chimeric gene. The constructed synthetic oligonucleotides encoded the same amino acid sequences and contained arginine codons AGG, AGA and CGT in various combinations. It was shown that the presence of rare arginine codons AGG and AGA in the template and their mutual arrangement significantly influence the level of gene expression. At the same time the presence of leucine, isoleucine, glycine and proline rare codons does not cause such an effect. Translation of AGGAGG and AGAAGA sequences was found to lead to the formation of a considerable amount of polypeptides of incomplete length. It was shown that the presence of such a cluster of rare codons effects on the length of specific mRNA.

Amino Acid Sequence↗
PubMed2003

[Association of the vitamin D receptor gene start codon polymorphism with vitamin D deficiency rickets].

OBJECTIVE: Vitamin D deficiency rickets often causes growth retardation, impaired bone formation and hypocalcemia in children. It is well known that rickets is mainly caused by vitamin D deficiency, but whether there is hereditary susceptibility of children to develop vitamin D deficiency rickets is unknown. Vitamin D receptor (VDR) gene has been used as one of genetic markers in studying the metabolic diseases of bone. The present study aimed to explore the hereditary susceptibility of children to develop rickets through studying the association between VDR gene start codon polymorphism and vitamin D deficiency rickets, METHODS: The subjects were selected from Kunming city, every subject was of Han ethnic group. The subjects were composed of two groups, the patient group consisted of 48 children with active vitamin D deficiency rickets which was diagnosed clinically and confirmed radiologically; the control group was composed of 92 normal children. Polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP), DNA sequence analysis and genetic analysis methods were used. A restriction fragment length polymorphism in the start codon of VDR gene (FokI) was tested in both groups. RESULTS: VDR gene start codon polymorphism was tested successfully for every subject. Frequencies of FF, Ff and ff genotypes were 46%, 33% and 21% in the rickets group, and 22%, 52% and 26% in the control group, respectively. A significant difference was found in the frequency distribution of VDR genotype between two groups (chi(2) = 8.912, P = 0.012). In the patient group, Ff and ff genotypes were less common than control group, but the FF genotype was more common than control group (OR = 3.046), indicating that FF genotype may be significantly associated with vitamin D deficiency rickets. Moreover, VDR allele frequencies of FokI polymorphism also showed significant difference between the two groups (chi(2) = 5.451, P = 0.020), F alleles were more common in patient group than in control group. DNA sequence analysis identified that the start codon of F allele was mutated from ATG to ACG. CONCLUSION: There is an association between VDR gene start codon polymorphism and vitamin D deficiency rickets. This study suggested the possibility that VDR gene polymorphism might be important in determining an individual's susceptibility to development of vitamin D deficiency rickets.

Base Sequence↗
PubMed2004

[Construction and immune potency of recombinant adenovirus containing codon-modified HIV-1 gp120].

BACKGROUND: To construct replication-deficient recombinant adenovirus expressing wild and codon-modified HIV-1 gp120. METHODS: The viral codons were changed to the codon usage of highly expressed mammal gene, the resulting modified gp120 gene was synthesized. The wild and modified gp120 genes were cloned into shuttle vector pShuttle-CMV respectively, and then the constructed plasmids containing gp120 gene was cotransformed with the backbone vector pADeasy-1 into E.coli BJ5183. Transfection of the recombinant AdEasy plasmid into 293 cells was performed to obtain recombinant adenoviruses. The mice were immunized with the recombinant adenoviruses. Their immunogenicity was evaluated by testing antibody and CTL levels of immunized mice. RESULTS: Two strains of recombinant adenovirus expressing wild and codon-modified HIV-1 gp120 were obtained. The protein expressing level of the recombinant adenoviruses containing modified genes was much higher than that containing wild genes. The mice immunized with recombinant adenoviruses elicited HIV-1 specific antibody and CTL response. The rAd-mod gp120 group was better than the rAd-wt gp120 group. CONCLUSION: Replication-deficient recombinant adenovirus expressing HIV-1 gp120 can elicit HIV-1 specific humoral and cellular response, the codon-modified recombinant virus was more efficient than the native.

AIDS Vaccines↗
PubMed2005

[Bias of base composition and codon usage in pseudorabies virus genes].

The complete sequence of the Pseudorabies Virus (PRV) genomic DNA has not yet been determined, primarily because of the high content of G + C nucleotides of about 74%. We examined the base composition and codon usage of the 68 known PRV genes. As a result, we found a strong bias towards GC-rich codons especially NNC or NNG (N represents any one of four nucleotides) in PRV genes. This demonstrated that the usage bias of synonymous codon and amino acid is the main cause of the high G + C content of PRV. The results showed that the genome regions adjacent UL48, UL40, UL14, IE180 genes where the G + C content occurs as pronounced waves are corresponding to the replication origins. It was also found that the codon usage patterns of regulatory genes are apparently different from other PRV genes. A corresponding analysis of amino acid compositions indicated that the bias of codon usage could be related to the differences of gene function.

Amino Acids↗
PubMed1990

Activation of K-ras by codon 13 mutations in C57BL/6 X C3H F1 mouse tumors induced by exposure to 1,3-butadiene.

1,3-Butadiene has been detected in urban air, gasoline vapors, and cigarette smoke. It has been estimated that 65,000 workers are exposed to this chemical in occupational settings in the United States. Lymphomas, lung, and liver tumors were induced in female and male C57BL/6 X C3H F1 (hereafter called B6C3F1) mice by inhalation of 6.25 to 625 ppm 1,3-butadiene for 1 to 2 years. The objective of this study was to examine these tumors for the presence of activated protooncogenes by the NIH 3T3 transfection and nude mouse tumorigenicity assays. Transfection of DNA isolated from 7 of 9 lung tumors and 7 of 12 liver tumors induced morphological transformation of NIH 3T3 cells. Southern blot analysis indicated that the transformation induced by 6 lung and 3 liver tumor DNA samples was due to transfer of a K-ras oncogene. Four of the 7 liver tumors that were positive upon transfection contained an activated H-ras gene. The identity of the transforming gene in one of the lung tumors has not been determined but was not a member of the ras family or a met or raf gene. Eleven 1,3-butadiene-induced lymphomas were examined for transforming genes using the nude mouse tumorigenicity assay. Activated K-ras genes were detected in 2 of the 11 lymphomas assayed. DNA sequencing of polymerase chain reaction-amplified ras gene exons revealed that 9 of 11 of the activating K-ras mutations were G to C transversions in codon 13. One liver tumor contained an activated K-ras gene with mutations in both codons 60 and 61. The activating mutation in one of the K-ras genes from a lymphoma was not identified but DNA sequence analysis of amplified regions in proximity to codons 12, 13, and 61 demonstrated that the mutation was not located in or near these codons. Activation of K-ras genes by codon 13 mutations has not been found in any lung or liver tumors or lymphomas from untreated B6C3F1 mice. Thus, the K-ras activation found in 1,3-butadiene-induced B6C3F1 mouse tumors probably occurred as a result of genotoxic effects of this chemical. The oncogenes most frequently detected in human pulmonary adenocarcinomas are K-ras genes. Activated K-ras genes have also been found in some human lymphomas. This suggest that activation of K-ras may be important in the induction of human pulmonary adenocarcinomas and lymphomas.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1989

Replication blocks and sequence interaction specificities in the codon 12 region of the c-Ha-ras proto-oncogene induced by four carcinogens in vitro.

We have examined the region surrounding codon 12 in the human c-Ha-ras proto-oncogene in vitro to determine the reaction intensities at the guanine nucleotides after exposure to the mycotoxin aflatoxin B1, to one of its human metabolites aflatoxin M1, to dimethyl sulfate, and to the major ultimate carcinogen of benzo(a)pyrene, benzo(a)pyrene diol-epoxide. Among the adducts produced, those at N-7-guanyl sites are alkali-labile and can be identified using a variation of the Maxam-Gilbert sequencing procedure. Data indicate that the guanine nucleotides of codon 12 have above average potential for adduct formation by the genotoxins when compared to other guanine sites, but were not the strongest sites. This codon 12 region has been inserted into single-stranded M13 phage, exposed to several of the genotoxins, and used as a template for DNA synthesis in vitro. There is a sequence-specific variation in polymerase inhibition at various adducted nucleotide sites, but replication blocks are not preferentially seen at the carcinogen-adducted guanines of codon 12. These results indicate that the predominance of point mutations which are detected in vivo at codon 12 do not reflect sequence-mediated preferential susceptibility of these sites to initial DNA adduction or to replication errors. The mechanisms controlling these sequence effects are not currently understood, and attempts to predict relative alkylation or termination frequencies based solely on local DNA sequence are not reliable.

Aflatoxin B1↗
PubMed1984

[Demonstration of a sudden change in the use of codons in the vicinity of transcription termination].

A characteristic profile of fluctuations in the use of codons is seen in bacteriophages, Mammal mitochondria and animal viruses. Following DNA in the direction of transcription, one goes slowly from an area rich in codons ending by C to an area rich in codons ending by T and then one falls abruptly in an area rich in C. The termination of transcription is located in the area where the use of codons changes suddenly. It seems that the choice of codons ending by T or C is directed by the necessity to have a variation in the stability of the DNA. We propose a dynamic model where large scale variations of the stability of the DNA regulates the speed of propagation of the RNA-polymerase.

Animals↗
PubMed1984

Beta O-39 thalassemia gene: a premature termination codon causes beta-mRNA deficiency without affecting cytoplasmic beta-mRNA stability.

The function of a beta O-thalassemia globin gene with a premature termination codon at position 39 was studied in tissue culture cells using plasmid expression vectors. The thalassemic globin gene was isolated by molecular cloning from the bone marrow DNA of an Italian patient with severe thalassemia. Sequences upstream of the normal beta-globin gene and the beta O-39 globin gene were removed to 127 nucleotides (nt) 5' to the start site of transcription, thereby eliminating uncharacterized DNA sequences but preserving promoter function. To create a hybrid gene differing from the normal by only the single nt change in codon 39, the truncated 5' end of the beta O-39 gene was recombined with the 3' end of the normal gene. The beta O-39 substitution resulted in a 6-14-fold reduction in cytoplasmic RNA accumulation in transfected monkey kidney or HeLa cells. This decrease in mRNA did not appear to be due to instability, as the beta-mRNA present 24-36 hours after transfection was stable for up to 24 hours in the presence of actinomycin D. In the presence of actinomycin D, the globin mRNA precursor disappeared, suggesting that globin gene transcription had been effectively blocked. We also examined a second globin mRNA with a premature termination codon; this RNA that arises from incorrect splicing of the transcript of a beta + -24 thalassemia gene was as stable as the correctly spliced species. Thus, the presence of a premature termination codon does not necessarily alter cytoplasmic mRNA stability, nor does cytoplasmic instability account for the quantitative deficiency of beta-globin mRNA. Our observations suggest that a premature termination codon alters intranuclear stability and/or nuclear to cytoplasmic transport of the beta-globin mRNA.

Codon↗
PubMed1995

Mutation screening of the codon 3500 region of the apolipoprotein B gene by denaturing gradient-gel electrophoresis.

Familial defective apolipoprotein B (FDB) is a clinical condition resembling familial hypercholesterolemia. The underlying genetic defects are mutations in the apolipoprotein B-100 (apo B-100) gene. Two mutations (Arg3500 --> Gln and Arg3531 --> Cys) are known to date. We designed a denaturing gradient-gel electrophoresis (DGGE) technique to detect sequence variations in codons 3456-3553 of the apo B-100 gene. In 46 heterozygous FDB patients with the predominant codon 3500 mutation, a uniform four-band DGGE pattern was seen, whereas 57 non-FDB patients showed the uniform single-band pattern expected in normal homozygotes. The recently described codon 3531 mutation and a previously unpublished Arg --> Pro mutation in codon 3480 showed unique DGGE patterns, allowing unambiguous differentiation of the three mutations. The DGGE method thus both detects known FDB mutations and screens for other mutations in codons 3456-3553 of the low-density lipoprotein receptor binding region of apo B-100; it can be used as a first-line screening method for FDB.

Apolipoprotein B-100↗
PubMed1994

Mutagenesis of codon 248 of the human p53 tumor suppressor gene by N-ethyl-N-nitrosourea.

Base pair mutations in the p53 tumor suppressor gene are among the most frequently observed genetic changes in human malignancies. Several mutational hotspots have been identified and tumor- and tissue-specific differences have been observed. We studied the mutability of hotspot codon 248, CGG, in human fibroblasts in response to the alkylating agent N-ethyl-N-nitrosourea (ENU) by MspI RFLP/PCR analysis. Alkylating agents are implicated as etiological agents in carcinogenesis in the gut and other tissues in the human. ENU induced preferentially G to A transitions in the non-transcribed strand. The predominant mutation involving the G-residue of the CpG dinucleotide was observed with an absolute frequency of 4 x 10(-7). The corresponding C to T transition in the first position of codon 248 was observed at several fold lower frequency suggesting more efficient excision repair of the transcribed strand. The G to A transition in the third position of codon 248 occurred at low frequency. Our results are compatible with a role for aliphatic alkylating agents in human tumors with codon 248 mutations since almost all mutations reported in this codon are transitions in the CpG-dinucleotide.

Base Sequence↗
PubMed1993

[Sensitive detection of K-ras oncogene codon 12 mutations by nested PCR using mismatched primers and selective digestion of non-mutated PCR fragments with restriction enzyme].

Sensitive detection of K-ras oncogene mutation at codon 12 using nested polymerase chain reactions (PCR) with mismatched primers combined with selective digestion of nonmutated DNA fragments after the first PCR amplification was reported by Levi S, et al. (Cancer Res 51:3497-3502, 1991). We examined the usefulness of this novel technique in cell lines carrying various K-ras codon 12 mutations and clinical samples such as colon carcinoma tissue, corresponding normal colonic mucosa and pancreatic juice obtained from the patients with pancreatic carcinoma undergoing endoscopic retrograde pancreatography (ERP). In analysis of tumor cell lines carrying mutated K-ras at codon 12, the fragment length of the amplified DNA was 135 bp after digestion using restriction enzyme BstN1, whereas those of nonmutated cell lines were 106 bp. This method was highly sensitive to detect mutant DNA diluted at a ratio of 2048 fold with normal DNA samples obtained from peripheral blood lymphocytes. In analysis of clinical samples, 4 out of 10 colorectal carcinoma tissues were positive for K-ras gene mutation at codon 12, however, no mutations were detected in corresponding normal colonic mucosa. In analysis of pancreatic juice taken from the patients with pancreatic carcinoma, 1 out of 3 samples were positive for K-ras mutation at codon 12. Thus, this novel approach was thought to be useful for detection of minimum number of cancer cells from compound samples containing larger amounts of normal cells.

Cells, Cultured↗
PubMed1976

[Composition and variability of bases in degenerate and non-degenerate positions in codons of various types of mRNA].

Codon base frequencies have been studied in all published mRNA sequences of more than 50 codons. Bases are not "random" in any codon position. Variability in degenerate position III is of the same order as in the other two positions (non-degenerate). The base distribution in each codon position is significantly different from that in each other position. Position I has the most distinctive make up. Correlations demonstrate that in this ensemble of 1,265 codons positions I and II have the same type of composition as in the decoded mRNA for the average protein.

Base Sequence↗
PubMed1996

Internal initiation of translation of hepatitis C virus RNA: the ribosome entry site is at the authentic initiation codon.

Hepatitis C viral (HCV) RNA includes an internal ribosome entry segment (IRES) that extends some 30 nt into the coding region and promotes internal initiation of translation at the authentic initiation codon at nt 342. The 5'-boundary of this IRES was mapped by in vitro translation and transfection assays and was found to lie between nt 42 and 71. Within these IRES boundaries there are, in most HCV strains, three AUG triplets upstream of the authentic initiation site. Although the first, 5'-proximal, of these is absolutely conserved, a mutational analysis showed that it is not a functional initiation codon. In particular, the G residue could be substituted provided compensatory mutations were made to maintain base pairing. The other two upstream AUGs are not absolutely conserved, and mutation of the third (5'-distal) had little effect on IRES activity. When an additional AUG codon was introduced by single-site mutation just upstream of the authentic initiation codon, it was found to be used when most of the IRES had been deleted to generate an RNA translated by the scanning ribosome mechanism, but was not used in the background of the full-length IRES when internal initiation is operative. These results argue that the IRES promotes direct ribosome entry immediately at, or indeed very close to, the authentic initiation codon, and that the upstream AUGs do not serve as ribosome entry sites.

Base Sequence↗
PubMed1998

Heterogeneity of mutant versus wild-type Ki-ras in primary and metastatic colorectal carcinomas, and association of codon-12 valine with early mortality.

The point mutations occurring in codons 12 and 13 of Ki-ras in 78 patients with colorectal carcinoma (31 Dukes' A and B, 21 Dukes' C, and 26 Dukes' D) have been determined by allele-specific oligonucleotide hybridization and sequencing. Duplicate samples of invasive primary carcinoma, adjacent normal tissue, and available lymph node and liver metastases from the same patients were microdissected from paraffin sections. There were no differences in the mutation rate between primary carcinomas and secondary deposits: 26 of 78 (33 per cent) primary carcinomas, 10 of 32 (31 per cent) lymph node metastases, and 10 of 26 (38 per cent) liver metastases. Multiple sampling revealed frequent heterogeneity within carcinomas: 9 of 26 primaries with Ki-ras mutations also contained areas of carcinoma with only the wild-type gene, implying that Ki-ras mutation, even when present in a colonic carcinoma, may not have been necessary for establishing the malignant phenotype. Also, 2 of 26 (8 per cent) Dukes' D patients had a mutation in their primary carcinoma but none in liver metastases and 6 of 47 (13 per cent) Dukes' C and D patients had mutations in liver or lymph node metastases but none in the primary carcinoma. Such heterogeneity may modify the effectiveness of novel therapies targeting mutant Ki-ras function, such as farnesyltransferase inhibition. Mutation of codon 12 from GGT (glycine) to GTT (valine) was more prevalent in primary and metastatic deposits of Dukes' C/D carcinomas (P = 0.01) than in primary carcinomas from Dukes' A/B patients. Mutations of codon 12 to GAT, AGT, GCT and codon 13 GGC to GAC were also found, but no correlation with carcinoma aggressiveness was apparent. Follow-up of 71/78 patients (up to 12 years) revealed decreased overall survival (P = 0.001) in patients with the GGT to GTT transversion in codon 12, even when the analysis was restricted to Dukes' D cases, supporting the suggestion that this mutation may confer a more aggressive phenotype in colorectal carcinoma.

Adenocarcinoma↗