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C Martinet

Publications and source records attributed to C Martinet.

At least 37 records · Page 2Linked to original sources
PubMed1977

Temperature-sensitive defect of vesicular stomatitis virus in complementation group II.

The prototype member of the complementation group II temperature-sensitive (ts) mutants of vesicular stomatitis virus, ts II 052, has been investigated. In ts II 052-infected HeLa cells at the restrictive temperature (39.5 degrees C), reduced viral RNA synthesis was observed by comparison with infections conducted at the permissive temperature (30 degrees C). It was found that for an infection conducted at 39.5 degrees C, no 38S RNA or intracytoplasmic nucleocapsids were present. For nucleocapsids isolated from ts II 052 purified virions or from ts II 052-infected cells at 30 degrees C, the RNA was sensitive to pancreatic RNase after an exposure at 39.5 degrees C in contrast to the resistance observed for wild-type virus. The nucleocapsid stability of wild-type virus when heated to 63 degrees C or submitted to varying pH was not found in nucleocapsids extracted from ts II 052 purified virions. The data suggest that for ts II 052 there is an altered relationship between the viral 38S RNA and the nucleocapsid protein(s) by comparison with wild-type virus. Such results argue for the complementation group II gene product being N protein, so that the ts defect in ts II 052 represents an altered N protein.

Genes↗
PubMed1974

Transcription and replication of vesicular stomatitis virus: effects of temperature-sensitive mutations in complementation group IV.

Temperature-sensitive (ts) mutants of vesicular stomatitis virus belonging to the RNA(-) complementation group IV were investigated under various conditions to study both their RNA and protein syntheses. In infected cells maintained at 39.2 C, viral RNA species were recovered only in the 13 to 15S region of the gradient in an amount depending on the ts mutant used. In the presence of cycloheximide at 39.2 C, the primary transcription was deficient, especially for 28S mRNA production. When mutant-infected cells were shifted to nonpermissive temperature, a shutoff of 28S mRNA synthesis occurred as a general feature. On the contrary under this condition, the two mutants chosen, ts IV100 and ts IV111, behaved very differently in their 13 to 15S and 38S RNA production. However, treatment with cycloheximide at the time of the transfer to 39.2 C resulted in a similar recovery of 13 to 15S RNA in both mutants, whereas the 28S remained very depressed. The viral proteins synthesized by cells infected with the same two mutants also showed a distinct pattern, especially regarding the N protein; a correlation between 38S RNA and protein N syntheses was tentatively drawn. The whole set of data suggested that the lesion in group IV mutants concerned a viral structural protein required for the process of in vivo transcription and which probably intervened in the replication mechanism.

Animals↗
PubMed1972

Study of the transcription and the replication of vesicular stomatitis virus by using temperature-sensitive mutants.

The viral ribonucleic acids (RNA species) synthesized in HeLa cells infected with temperature-sensitive (ts) mutants and with the wild type of vesicular stomatitis virus at permissive (30 C) and nonpermissive (39.2 C) temperatures were compared by sucrose gradient centrifugation. Two ts mutants (ts 5 and ts 100) representing two separate complementation groups (respectively, groups I and IV), each concerned with viral RNA synthesis, were chosen. Mutant ts 5 failed to synthesize any RNA at 39.2 C. Under the same conditions, mutant ts 100 showed a low, but easily detectable, synthesis of RNA without characteristic peaks. The in vitro transcriptase activity was tested with mutants ts 5 and ts 100 at 39.2 C: normal activity, compared with wild-type virus, was detected with purified ts 100, but no activity was detected with purified ts 5. From all our data we conclude that mutant ts 5 is defective in transcription. The defect could be in the structural transcriptase enzyme or at the level of template for transcription. Results with mutant ts 100 were not so clear-cut. However, we suggest that this mutant is concerned with some aspect of transcription in vivo. In addition, our results lead us to postulate some linkage between transcription and replication.

Cell-Free System↗
PubMedDate not supplied

[Muir-Torre syndrome and familial colorectal cancer: 2 families with molecular genetic analysis].

INTRODUCTION: The Muir-Torre Syndrome is a rare genodermatosis, defined by the occurrence of cutaneous tumors (such as sebaceous adenomas, epitheliomas, or carcinomas, and/or keratoacanthomas), and internal malignancies. Recently, molecular analysis in hereditary non polyposis colorectal cancer demonstrated a common genetic basis, linking these two disorders, with the observation of germline mutations in the hMSH2 gene (one of the DNA mismatch repair system genes) in both syndromes. Such molecular demonstration of a single nosological entity should be clinically used to improve the indications of molecular testings in oncogenetics, still restricted to highly stringent criteria for hereditary non polyposis colorectal cancer. CLINICAL CASES: We identified three patients from two different families, who fulfilled the criteria for both Muir-Torre Syndrome and hereditary non polyposis colorectal cancer. The search of a germline mutation of the hMSH2 gene was performed on an affected member from each family, and their relatives with their informed consent. Within each family, all individuals with colorectal cancer were carriers of the same mutation. In the first family, this mutation was a pathogenic microinsertion, usable for predictive testing. In the second family, a missense mutation was identified, requesting further demonstration of its pathogenicity before its use in a predictive purpose. CONCLUSIONS: The diagnosis of cutaneous tumors compatible with Muir-Torre syndrome should lead the dermatologist to suspect an hereditary non polyposis colorectal cancer that should bring to an oncogenetic approach: personnal and familial history of colorectal cancer, molecular analysis, recommendations for colonoscopic screening in at-risk relatives. In the case of a colorectal cancer at a young age, or in the case of familial cases, the gastroenterologist should screen for cutaneous lesions of Muir-Torre syndrome, which could add a criteria for an hereditary syndrome, and lead to molecular oncogenetic analysis.

Adenoma↗