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Biomedical subjects

T Shenk

Publications and source records attributed to T Shenk.

153 records · Page 9Linked to original sources
PubMed1979

Isolation of adenovirus type 5 host range deletion mutants defective for transformation of rat embryo cells.

A series of adenovirus type 5 (Ad5) deletion, insertion and substitution mutants, some of which are defective for transformation of rat cells, have been isolated. The mutants were selected as variants which lack the Xba I endonuclease cleavage site at 4 map units on the viral chromosome. The deletions range in size from 150-2300 bp and are located between 1.5 and 10.5 map units. The mutants can be propagated in 293 cells (Ad5-transformed human embryonic kidney cells), but are defective for growth in HeLa or human embryonic kidney cells. No viral DNA synthesis was observed in mutant virus-infected HeLa cells. All but one of the deletion mutants tested were defective for transformation of rat embryo and rat embryo brain cells.

Adenoviridae↗
PubMed1979

An adenovirus type 5 early gene function regulates expression of other early viral genes.

We have identified an adenovirus type 5(Ad5) early gene function located in early region 1 which is required for the production of early cytoplasmic mRNAs corresponding to early regions 2, 3, and 4. Mutant dl312 (lacks the segment between 1.5 and 4.5 map units) grows as well as wild-type virus in 293 cells (Ad5-transformed human embryonic kidney cells), but its growth is severely restricted in HeLa cells. We detect no viral RNAs in the cytoplasm of dl312-infected HeLa cells. Viral RNA sequences are present, however, in dl312-infected HeLa cell nuclei.

Adenoviruses, Human↗
PubMed1979

Nucleotide sequence analysis of viable deletion mutants lacking segments of the simian virus 40 genome coding for small t antigen.

The deletions in nine viable simian virus 40 mutants have been mapped by direct DNA sequence analysis. The mutant DNAs lack small segments of the early region of the viral chromosome (between 0.535 and 0.600 map unit). The deletions are all located in the region which is removed from the large T antigen transcript by splicing. No one deletion removes this entire region, but no part of this segment is conserved in all of the mutants except for several nucleotides near the splice points of the transcript. Although the deletions do not alter the region coding for the large T polypeptide, they do delete portions of the segment coding for the C-terminal half of the small t polypeptide.

Antigens, Viral↗
PubMed1978

Construction of a viable SV40 variant containing two functional origins of DNA replication.

Viable variants of simian virus 40 (SV40) have been constructed which contain two functional origins of DNA replication (Or). The variants were made by introducing, at 0.175 on the SV40 map, a segment of DNA containing the viral Or. Two types of experiments demonstrate that the second Or is functional. First, the distribution of radioactivity in pulse-labeled SV40 (I) DNA is dramatically altered in the variants when compared with the parental virus. Second, electron microscopic examination of viral replicative intermediates indicates that while there is one initiation site for DNA synthesis in the parental genome, there are two sites in the variant. It was possible to introduce a deletion which inactivated the original Or at 0.67 map units in this variant. The resulting mutant could be propagated, and its DNA replication originated at the site of the newly inserted Or.

DNA Replication↗
PubMed1978

New region of the simian virus 40 genome required for efficient viral transformation.

Viable mutants of simian virus 40 with deletions in three regions of the virus genome (map coordinates 0.21-0.17, 0.59-0.54, and 0.67-0.74) have been tested for their ability to transform rat fibroblasts to anchorage independence. Only those mutants whose deletions occur between 0.59 and 0.55 in the proximal part of the early region are defective in transforming ability. The most severely defective of these transform with less than one-hundredth the efficiency of wild type. They retain their defect when tested in Chinese hamster lung cells and when infection is initiated with viral DNA instead of intact virions. Complementation for transformation can be observed between these transformation-defective deletions and a simian virus 40 temperature-sensitive A mutant.

Cell Line↗
PubMed1978

Definition of the boundaries of the origin of DNA replication in simian virus 40.

We have determined by use of DNA sequencing techniques the exact location of the deletion in d1 892, a viable deletion mutant of Simian virus 40 (SV40) reported to map very near the unique replication origin or SV40. With the help of this localization we have narrowed down the boundaries of the replication origin to 85 nucleotides within the sequence of SV40.

Base Sequence↗