Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.1.27.3 (RNase T1)
1,228 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A procedure has been developed to map the genetic elements of avian tumor virus RNA, which has a molecular weight of about 3 X 10(6) daltons and a poly(A) sequence at the 3' end. For this purpose, about 30 RNase T1-resistant oligonucleotides were ordered relative to the 3'-poly(A) terminus of the RNA, to construct an oligonucleotide map of viral RNAs. A cluster of seven envelope gene (env)-specific oligonucleotides, identified by their absence from the otherwise very similar oligonucleotide map of an envelope-defective deletion mutant (which lacks the major viral glycoprotein), mapped at a distance of 0.9 to 1.6 X 10(6) daltons from the poly(A) end of sarcoma virus RNA. A cluster of three sarcoma gene (src)-specific oligonucleotides, identified by their absence from the otherwise nearly identical oligonucleotide map of a transformation-defective deletion mutant mapped at a distance of 0.2 to 0.6 X 10(6) daltons from the poly(A) end of sarcoma virus RNA. The oligonucleotide maps of sarcoma viruses and of related deletion mutants were the same from the poly(A) end up to 0.2 X 10(6) daltons and included one terminal oligonucleotide, termed C, which is found in all avian tumor viruses tested so far. Preliminary mapping experiments ordering the src-specific and env-specific oligonucleotides of recombinants, selected for sarcoma and envelope genes of different parents, agree with those obtained by comparing maps of wild type viruses and deletion mutants. A partial genetic map consistent with these results suggests that the src gene maps between the env gene and the 3'-poly(A) end of viral RNA. This map reads: poly(A)-src-env-(pol, gag).
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PMID:Sequences and functions of Rous sarcoma virus RNA. 18 29

The RNA of myelocytoma virus MC29, a replication-defective avian acute leukemia virus, was investigated. Sedimentation and electrophoretic analyses indicated that the virus contains a distinct 28S RNA with about 5700 nucleotides. It is the smallest avian tumor virus RNA detected to date. The small size of the RNA suggests that the defectiveness of the virus is due to deletions in replicative genes. The RNA shared 3 to 5 of 30 large RNase T1-resistant oligonucleotides with the RNA of other avian leukosis and sarcoma and may represent the transforming information of the virus. Sequences of the conserved transforming gene of avian sarcoma viruses were not detected in MC29 RNA. It was concluded that the transforming sequences of MC29 RNA define a new class of avian tumor viral transforming genes.
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PMID:The RNA of avian acute leukemia virus MC29. 20 Sep 13

Three RNA fractions with molecular weights of 200,000, 280,000, and 360,000, have been identified as the major polyadenylylated transcription products in a transplantable rat pancreatic islet cell tumor that synthesizes insulin. These three RNAs share sequence homology as demonstrated by comparisons of both partial and complete RNase T1 digestion products. The 200,000 and 280,000 molecular weight species hybridize primarily with three EcoRI restriction fragments of the rat genome having molecular weights of 1.4 X 10(6), 1.6 X 10(6), and 6.0 X 10(6). The 360,000 molecular weight species hybridizes preferentially with the 6.0 X 10(6) molecular weight DNA fragment.
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PMID:Identification of the major polyadenylylated transcription products and the genes active in their synthesis in a rat insulinoma. 21 Apr 56

The genome of the defective avian tumor virus MH2 was identified as a RNA of 5.7 kilobases by its presence in different MH2-helper virus complexes and its absence from pure helper virus, by its unique fingerprint pattern of RNase T1-resistant (T1) oligonucleotides that differed from those of two helper virus RNAs, and by its structural analogy to the RNA of MC29, another avian acute leukemia virus. Two sets of sequences were distinguished in MH2 RNA: 66% hybridized with DNA complementary to helper-independent avian tumor viruses, termed group-specific, and 34% were specific. The percentage of specific sequences is considered a minimal estimate because the MH2 RNA used was about 30% contaminated by helper virus RNA. No sequences related to the transforming src gene of avian sarcoma viruses were found in MH2. MH2 shared three large T1 oligonucleotides with MC29, two of which could also be isolated from a RNase A- and T1-resistant hybrid formed between MH2 RNA and MC29 specific cDNA. These oligonucleotides belong to a group of six that define the specific segment of MC29 RNA described previously. The group-specific sequences of MH2 and MC29 RNA shared only the two smallest out of about 20 T1 oligonucleotides associated with MH2 RNA. It is concluded that the specific sequences of MH2 and MC29 are related, and it is proposed that they are necessary for, or identical with, the onc genes of these viruses. These sequences would define a related class of transforming genes in avian tumor viruses that differs from the src genes of avian sarcoma viruses.
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PMID:Avian acute leukemia viruses MC29 and MH2 share specific RNA sequences: evidence for a second class of transforming genes. 22

Tumors were produced in quails about 2 months after injection with a transformation-defective mutant of the Schmidt-Ruppin strain of Rous sarcoma virus, subgroup A (SR-A), that retains a small portion of the src gene. Sarcoma viruses were isolated from each of five such tumors. A transformation-defective mutant which has a nearly complete deletion of the src gene was unable to induce tumors. The avian sarcoma viruses recovered from quail tumors (rASV-Q) had biological properties similar to those of the avian sarcoma viruses previously acquired from chicken tumors (rASV-C); these chicken tumors had been induced by the same transformation-defective mutants. Both rASV-Q and rASV-C transformed cells in culture with similar focus morphology and produced tumors within 7 to 14 days after injection into chickens or quails. The size of rASV-Q genomic RNA was indistinguishable from that of SR-A by polyacrylamide gel electrophoresis. The sequences of rASV-Q RNA genomes were analyzed and compared with those of the parental transformation-defective virus, SR-A and of rASV-C by RNase T1 fingerprinting and oligonucleotide mapping. We found that the src sequences of all five isolates of rASV-Q were identical to each other but different from those of SR-A and rASV-C. Of 13 oligonucleotides of rASV-Q identified as src specific, two were not found in either SR-A or rASV-C RNA. Furthermore, some oligonucleotides present in SR-A or rASV-C or both were absent in rASV-Q. No differences were found for the sequences outside the src region in any of the viruses examined. In addition, rASV-Q-infected cells possessed a 60,000-dalton protein specifically precipitable by rabbit serum raised against SR-D-induced tumors. The facts that the src sequences are essentially the same for rASV's recovered from one animal species and different for rASV's obtained from different species provide conclusive evidence that cellular sequences of normal birds were inserted into the viral genome and supplied to the resulting recombinant viruses genetic information for cell transformation.
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PMID:Analysis of the src gene of sarcoma viruses generated by recombination between transformation-defective mutants and quail cellular sequences. 22 78

The RNA species of the defective avian acute leukemia virus MC29 and of the defective avian carcinoma virus MH2 and of their helper viruses were analyzed using gel electrophoresis, fingerprinting of RNase T1-resistant oligonucleotides, RNA-cDNA hybridization and in vitro translation. A28S RNA species, of 5700 nucleotides, was identified as MC29- or MH2-specific. MC29 RNA shared 4 out of about 17 and MH2 RNA at least 1 out of 16 T1-oligonucleotides with several other avain tumor virus RNAs. In addition MC29 and MH2 RNAs shared 2 oligonucleotides which were not found in any other viral RNA tested. 60% of each 28S RNA could be hybridized by DNA complementary to other avian tumor virus RNAs (group-specific) but 40% could only be hybridized by homologous cDNA (specific). Src gene-related sequences of Rous sarcoma virus were not found in MC29 or MH2 RNA. The specific and group-specific sequences of MC29, defined in terms of their T1-oligonucleotides, were located on a map of all T1-oligonucleotides of viral RNA. Specific sequences mapped between 0,4 and 0,7 map units from the 3'poly(A) end and group-specific sequences mapped between 0 and 0,4 and 0,7 and 1 map units. The MC29-specific RNA segment was represented by 6 oligonucleotides, two of which were those shared only by MC29 and MH2 RNAs. In vitro translation of MC29 RNA generated a major 120 000 dalton protein and minor 56 000 and 37 000 dalton proteins. The 120 000 dalton protein shared sequences with the proteins of the avian tumor viral gag gene, which maps at the 5' end of independently replicating viruses. Since a gag gene-related oligonucleotide was also found near the 5' end of MC29 RNA, we propose that the 120 000 MC29 protein was translated from the 5' 60% of MC29 RNA. It would then include sequences of the defective gag gene as well as MC29-specific sequences. Since both MC29 and MH2 lack the src (sarcoma) gene of Rous sarcoma virusk it is concluded that they contain a distinct class of transforming (onc) genes. We propose that the specific sequences of MC29 and MH2 represent all, or part of, their onc genes because the onc genes of MC29 and MH2 are specific and represent the only known genetic function of these viruses. If this proposal is correct, the onc genes of MC29 and MH2 would be related, because the specific RNA sequence of MC29 shares 2 of 6 oligonucleotides with MH2. It would also follow that the 120 000 dalton MC29 protein is a probable onc gene product, because it is translated from MC29-specific (and group-specific) sequences and because both MC29- and MH2-transformed cells contain specific 120 000 and 100 000 dalton proteins, respectively.
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PMID:Anatomy of the RNA and gene products of MC29 and MH2, two defective avian tumor viruses causing acute leukemia and carcinoma: evidence for a new class of transforming genes. 23 56

The RNAs of several avian tumor virus recombinants that had inherited their focus-forming ability from a sarcoma virus and their host range marker from a leukosis virus were investigated. Electrophoretic analyses showed that the cloned sarcoma virus recombinants contained only size class a RNA, although they had acquired a marker that resided on class b RNA in the leukosis virus parent. Class a RNA of different recombinant clones, derived from the same pair of parental viruses and selected for the same biological markers, differed slightly in electrophoretic mobility from each other and from the parental sarcoma virus. They were also found to have different fingerprints of RNase T1-resistant oligonucleotides. The average complexity of the 60-70S RNA prepared from Prague Rous sarcoma virus of subgroup B was estimated to be 3.5 x 10(6) daltons from the size of 20 RNase T1-resistant oligonucleotides, which represented 3.9% of the RNA and that of a recombinant to be 3.3 x 10(6) daltons from 23 oligonucleotides, which represented 4.7% of the RNA. This result suggests that the genome of wild-type and of recombinant RNA tumor viruses is polyploid. The sum of these observations led us to propose that recombination among avian tumor viruses occurred by crossing-over between homologous pieces of nucleic acid.
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PMID:Evidence for crossing-over between avian tumor viruses based on analysis of viral RNAs. 437 15

Simian virus 40 (SV40) large tumor (T) antigen isolated from mammalian cells undergoing lytic or transforming infection is associated with small RNA fragments ("T-antigen RNA") that are protected from nuclease digestion. The rather high complexity of the ribonuclease T1 fingerprints of T-antigen RNA suggested that it is mainly derived from cellular heterogeneous nuclear RNAs. In the present study, 5'-32P-labeled T-antigen RNA was hybridized to monkey, mouse, and human Alu and SV40 DNA, and the nucleotide sequence of 37 T1 oligonucleotides was determined. The results suggest that the bulk of T-antigen RNA is derived from noncoding, double-stranded, ordered regions of cellular heterogeneous nuclear RNAs that exhibit sequence homologies with interspersed repetitive elements of the cellular genome. The possible biological implications of these results are discussed.
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PMID:Nature and origin of the RNA associated with simian virus 40 large tumor antigen. 608 2

Chicken myeloblasts transformed by avian myeloblastosis virus (AMV) in the absence of nondefective helper virus (termed nonproducer cells) were found to release a defective virus particle (DVP) that contains avian tumor viral gag proteins but lacks envelope glycoprotein and a DNA polymerase. Nonproducer cells contain a Pr76 gag precursor protein and also a protein that is indistinguishable from the Pr180 gag-pol protein of nondefective viruses. The RNA of the DVP is 7.5 kilobases (kb) long and is 0.7 kb shorter than the 8.2-kb RNAs of the helper viruses of AMV, MAV-1 and MAV-2. Comparisons based on RNA.cDNA hybridization and mapping of RNase T1-resistant oligonucleotides indicated that DVP RNA shares with MAV RNAs nearly isogenic 5'-terminal gag and pol-related sequences of 5.3 kb and a 3'-terminal c-region of 0.7 kb that is different from that found in other avian tumor viruses. Adjacent to the c-region, DVP RNA contains a contiguous specific sequence of 1.5 kb defined by 14 specific oligonucleotides. Except for two of these oligonucleotides that map at its 5' end, this sequence is unrelated to any sequences of nondefective avian tumor viruses of four different envelope subgroups as well as to the specific sequences of fibroblast-transforming avian acute leukemia and sarcoma viruses of four different RNA subgroups. The specific sequence of the DVP RNA is present in infectious stocks of AMV from this and other laboratories in an AMV-transformed myeloblast line from another laboratory, and it is about 70% related to nucleotide sequences of E26 virus, an independent isolate of an AMV-like virus. Preliminary experiments show DVP to be leukemogenic if fused into susceptible cells in the presence of helper virus. We conclude that DVP RNA is the leukemogenic component of infectious AMV and that its specific sequence, termed AMV, may carry genetic information for oncogenicity. Thus we have found here a transformation-specific RNA sequence, unrelated to helper virus, in a highly oncogenic virus that does not transform fibroblasts.
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PMID:Genetic structure of avian myeloblastosis virus, released from transformed myeloblasts as a defective virus particle. 615 39

Previously we have isolated the specific RNA methyltransferase from the nucleoli of Ehrlich ascites tumor cells. The purified enzyme was found to be specific for methylation of C5 position of cytosine residue in ribosomal RNA in vitro (Obara, 1982b). In the present study, we have investigated the recognition mechanisms of RNA structure by this enzyme from the points of view of both primary and secondary structures. Analysis of in vitro methylation product by ribonuclease T1 digestion indicated the methylation-site(s) was limited to a certain number of nonanucleotide. The next experiments with either Sl nuclease or actinomycin D and ethidium bromide suggested that the enzyme modified only cytidine residue in or located close to the double stranded part of RNA. On the other hand, the characterization of analogues of cytidine residue in the RNA at molecular level showed that the methylation of rRNA was inhibited by either cytidine, CDP or CTP, but little inhibition was observed in the presence of cytosine, 5-methylcytidine and CMP.
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PMID:Recognition of the ribosomal RNA structures by purified nucleolar RNA methyltransferase. 667 41


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