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T Eremenko

Publications and source records attributed to T Eremenko.

28 records · Page 2Linked to original sources
PubMed1974

A guanidine-sensitive step of the poliovirus RNA replication cycle.

It has been shown that the amount of viral RNA synthesized in synchronized HeLa cells 0-2 h after infection does not notably vary during the mitotic cycle. However, the amount of viral RNA synthesized 2-4.5 h after infection exhibited a sharp maximum in S-phase cells. Guanidine inhibited the incorporation of 3-H-uridine into the viral RNA synthesized 2-4.5 h after infection only in cells in the S-phase. It had no demonstrable effect on viral RNA synthesis 0-2 h after infection in cells in any phase of the mitotic cycle. Thus, additional indirect evidence has been presented in favor of the hypothesis that two different replicases or two different conformations of one enzyme are involved in poliovirus RNA replication. The one functioning 0-2 h after infection is cycle-independent and guanidine-sensitive, whereas the other functions exclusively in phase-S cells 2-4.5 h after infection and is inhibited by guanidine.

Cell Division↗
PubMedDate not supplied

Repair-modification and evolution of the eukaryotic genome organization.

For a complete reconstruction of the damaged unmethylated islands, in theory, the conventional excision-repair is sufficient. For a complete reconstruction of the damaged methylated domains, a coupling has to take place involving the excision-repair (able to reestablish their ATGC-language) plus the DNA-methylase (able to reestablish their modified ATGC5mC-language). This coupling, defined as "repair-modification," is essentially functioning during the S-phase, because the DNA-polymerase beta (pol beta) is active during the whole cell cycle, whereas the DNA-methylase (met) is active in S and appears to be repressed or inactive during the major part of G1 and during the phases G2 and M. Consequently, after damage, some silent genes might become expressed during these phases, if it is true that DNA methylation is inversely proportional to transcription. Repair-modification should, therefore, exert a continuous differential pressure on evolution of given parts of the genome, when they are methylated to a different extent. According to Darwinian concepts, repair-modification would lead to a high variability, especially of uncoding DNA sequences (if hypermethylated), whereas on the basis of this variability, selection might favor transposition of specific regulatory elements into given transcriptional units. In these, the conservative nature of the coding elements (if unmethylated) would obviously be ensured by the conventional excision-repair.

Animals↗
PubMedDate not supplied

[Position of the attachment site of the SV40 virus genome at the transcription unit level].

DNA of OV40-transformed 3T3 cell line is more methylated than that of normal cells. Integrated sequences of OV40 DNA, however, are methylated less than the host DNA. Virus-specific sequences are flanked by highly methylated areas of cellular DNA of intron nature. The virus-specific pre-mRNA isolated from nuclei (28-37 S) is capable of hybridization with the low-methylated region of early OV40 genes coding for T-antigen, highly methylated exon containing a signal for polyadenylation and stop-codon. After processing, the virus-specific mRNA (19 S) extracted from polysomes loses the capacity of hybridization with highly methylated intron apparently due to splicing. On the other hand, the early gene of the virus is mapped in the A fragment obtained by combined hydrolysis of OV40 DNA with ECO RI, BamHI and Bg III. Because this fragment is shorter (2.6 Kb) than virus-specific mRNAs, it is assumed that T-antigen (mol. mass 94,000) is a hybrid protein containing amino acid sequences coded for by cellular DNA. From this point of view, integration of OV40 DNA leads to the formation of a "virus-cell transcription unit" for T-antigen, and multiple integration may be associated with repetition of the same target.

Animals↗