ON STRUCTURAL ORGANIZATION OF OPERON AND REGULATION OF RNA SYNTHESIS IN ANIMAL CELLS

A hypothesis on the structural organization of the operon in the cells of higher organisms is described. It is assumed that the operon in higher organisms consists of two main parts: promoter-proximal acceptor (or non-informative) zone and promoter-distal structural (or informative) zone. The non-informative zone contains acceptor loci, which do not carry any information but can specifically interact with certain proteins, predominantly with regulatory proteins. The informative zone contains structural genes and regulatory genes, carrying information regarding structural proteins, enzymes and regulatory proteins. Different operons may contain identical or similar acceptor loci, the most multiple acceptor loci being localized in the proximal part. On the other hand, one operon contains a number of different acceptor loci, reacting with different regulatory proteins. In the first stage the whole operon is transcribed and giant D-RNA is formed. Then the replica from the non-informative part degrades and the replica from structural genes (net mRNA's) are transferred into the cytoplasm. The combining of regulatory proteins with acceptor loci alters or prevents the movement of RNA polymerase along the operon and the transcription of the structural zone. This model gives a satisfactory explanation of a number of facts such as (1) the formation of giant D-RNA and R-RNA molecules and their further cleavage; (2) the existence of special nuclear D-RNA and R-RNA, degraded in the cell nucleus; (3) the role of a certain part of the DNA base sequence repetitions scattered throughout the genome; (4) the specific inhibition of repeated DNA base sequences by f 1 histone, etc. A number of conclusions and predictions are described which may be checked experimentally. In the light of the suggested hypothesis it is possible to explain the mechanism of tumour transformation, produced by oncogenic DNA-containing viruses and by some other factors. © 1997 Elsevier Science Ltd. All rights reserved.