Bacteriophage λ DNA fragments replicate in theParamecium macronucleus: Absence of active copy number control

1992 ◽  
Vol 13 (2) ◽  
pp. 97-102 ◽  
Author(s):  
Chung Sookkim ◽  
John R. Preer ◽  
Brry Polisky
Keyword(s):  
Copy Number ◽  
Dna Fragments ◽  
Bacteriophage Λ ◽  
Copy Number Control ◽  
Active Copy

Cloning of bacteriophage T5 DNA fragments in plasmid pBR322 and bacteriophage λ gtwes

Gene ◽  
1979 ◽  
Vol 8 (1) ◽  
pp. 53-68 ◽  
Author(s):  
Francoise Brunel ◽  
John Davison ◽  
Mireille Merchez
Keyword(s):  
Dna Fragments ◽  
Plasmid Pbr322 ◽  
Bacteriophage Λ ◽  
Bacteriophage T5

Broad Host-Range Plasmid R1162: Replication, Incompatibility, and Copy-Number Control

1985 ◽  
pp. 173-188 ◽  
Author(s):  
Richard J. Meyer ◽  
Lung-Shen Lin ◽  
Kyunghoon Kim ◽  
Michael A. Brasch
Keyword(s):  
Host Range ◽  
Copy Number ◽  
Broad Host Range ◽  
Copy Number Control ◽  
Broad Host Range Plasmid

Post-transcriptional Cosuppression of Ty1 Retrotransposition

Genetics ◽  
2003 ◽  
Vol 165 (1) ◽  
pp. 83-99
Author(s):  
David J Garfinkel ◽  
Katherine Nyswaner ◽  
Jun Wang ◽  
Jae-Yong Cho
Keyword(s):  
Gene Silencing ◽  
Reverse Transcription ◽  
Copy Number ◽  
Transcript Level ◽  
Gag Protein ◽  
Protein Levels ◽  
Copy Number Control ◽  
Gal1 Promoter ◽  
Pgk1 Promoter ◽  
Ty1 Retrotransposition

Abstract To determine whether homology-dependent gene silencing or cosuppression mechanisms underlie copy number control (CNC) of Ty1 retrotransposition, we introduced an active Ty1 element into a naïve strain. Single Ty1 element retrotransposition was elevated in a Ty1-less background, but decreased dramatically when additional elements were present. Transcription from the suppressing Ty1 elements enhanced CNC but translation or reverse transcription was not required. Ty1 CNC occurred with a transcriptionally active Ty2 element, but not with Ty3 or Ty5 elements. CNC also occurred when the suppressing Ty1 elements were transcriptionally silenced, fused to the constitutive PGK1 promoter, or contained a minimal segment of mostly TYA1-gag sequence. Ty1 transcription of a multicopy element expressed from the GAL1 promoter abolished CNC, even when the suppressing element was defective for transposition. Although Ty1 RNA and TyA1-gag protein levels increased with the copy number of expressible elements, a given element's transcript level varied less than twofold regardless of whether the suppressing elements were transcriptionally active or repressed. Furthermore, a decrease in the synthesis of Ty1 cDNA is strongly associated with Ty1 CNC. Together our results suggest that Ty1 cosuppression can occur post-transcriptionally, either prior to or during reverse transcription.

scholarly journals Erratum for Saha et al., Atrans-Dominant Form of Gag Restricts Ty1 Retrotransposition and Mediates Copy Number Control

2016 ◽  
Vol 90 (10) ◽  
pp. 5210-5210
Author(s):  
Agniva Saha ◽  
Jessica A. Mitchell ◽  
Yuri Nishida ◽  
Jonathan E. Hildreth ◽  
Joshua A. Arribere ◽  
...  
Keyword(s):  
Copy Number ◽  
Dominant Form ◽  
Copy Number Control ◽  
Ty1 Retrotransposition

scholarly journals A Flp-SUMO hybrid recombinase reveals multi-layered copy number control of a selfish DNA element through post-translational modification

PLoS Genetics ◽  
2019 ◽  
Vol 15 (6) ◽  
pp. e1008193 ◽  
Author(s):  
Chien-Hui Ma ◽  
Bo-Yu Su ◽  
Anna Maciaszek ◽  
Hsiu-Fang Fan ◽  
Piotr Guga ◽  
...  
Keyword(s):  
Copy Number ◽  
Post Translational Modification ◽  
Selfish Dna ◽  
Copy Number Control

scholarly journals The Papillomavirus E8∧E2C Protein Represses DNA Replication from Extrachromosomal Origins

2003 ◽  
Vol 23 (22) ◽  
pp. 8352-8362 ◽  
Author(s):  
Thomas Zobel ◽  
Thomas Iftner ◽  
Frank Stubenrauch
Keyword(s):  
Dna Replication ◽  
Dna Binding ◽  
Copy Number ◽  
Human Papillomaviruses ◽  
Virus Infections ◽  
Dimerization Domain ◽  
Barr Virus ◽  
Amino Terminal ◽  
Copy Number Control ◽  
Epstein Barr

ABSTRACT Carcinogenic DNA viruses such as high-risk human papillomaviruses (HPV) and Epstein-Barr-Virus (EBV) replicate during persistent infections as low-copy-number plasmids. EBV DNA replication is restricted by host cell replication licensing mechanisms. In contrast, copy number control of HPV genomes is not under cellular control but involves the viral sequence-specific DNA-binding E2 activator and E8∧E2C repressor proteins. Analysis of HPV31 mutant genomes revealed that residues outside of the DNA-binding/dimerization domain of E8∧E2C limit viral DNA replication, indicating that binding site competition or heterodimerization among E2 and E8∧E2C proteins does not contribute to copy number control. Domain swap experiments demonstrated that the amino-terminal 21 amino acids of E8∧E2C represent a novel, transferable DNA replication repressor domain, whose activity requires conserved lysine and tryptophan residues. Furthermore, E8∧E2C(1-21)-GAL4 fusion proteins inhibited the replication of the plasmid origin of replication of EBV, suggesting that E8∧E2C functions as a general replication repressor of extrachromosomal origins. This finding could be important for the development of novel therapies against persistent DNA tumor virus infections.

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