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Polyomavirus enhancer requirements for expression in embryonal carcinoma cells
1Department of Microbiology, Immunology and Molecular Genetics, Albany Medical College, NY 12208.
The International Journal of Developmental Biology
|March 1, 1993
Summary
New polyomavirus mutants overcome suppression in embryonal carcinoma cells, revealing a novel AP-1 binding site in the enhancer region crucial for viral expression and replication.
Area of Science:
- Virology
- Molecular Biology
- Cancer Research
Background:
- Wild type polyomavirus expression is suppressed in embryonal carcinoma (EC) cells but is alleviated upon differentiation.
- Host range mutants of polyomavirus can overcome this suppression and replicate in undifferentiated EC cells.
Purpose of the Study:
- To understand the function of mutations in polyomavirus host range mutants.
- To characterize rearrangements necessary for polyomavirus expression and replication in PCC4 cells.
Main Methods:
- Analysis of a new pyPCC4 isolate (LPT) derived without selection.
- Characterization of the B enhancer limits in PCC4 cells compared to permissive systems.
- Identification of sequence rearrangements and conserved features in host range mutants.
Main Results:
- A novel sequence with homology to the AP-1 core consensus sequence is found in 8 of 10 isolates within the enhancer region.
- The precise location of these junctions varies, suggesting a functional role.
- The origin proximal limit of the B enhancer for replication was located near nt 5189, and for transcription near nt 5215.
Conclusions:
- The identified AP-1-like sequence is a novel feature shared by polyomavirus mutants capable of expression in PCC4 cells.
- The distinct but overlapping enhancer cores for replication and transcription are conserved.
- These findings provide insight into the molecular mechanisms of polyomavirus host range and replication in EC cells.