Ribosomal DNA is one of the most conserved parts of the genome, especially in its rRNA coding regions, but some puzzling pieces of its noncoding repetitive sequences harbor secrets of cell growth and development machinery. Disruptions in the neat mechanisms of rDNA orchestrating the cell functioning result in malignant conversion. In cancer cells, the organization of rRNA coding genes and their transcription somehow differ from that of normal cells, but little is known about the particular mechanism for this switch. In this study, we demonstrate that the region ~2 kb upstream of the rDNA promoter is transcriptionally active in one type of the most malignant human brain tumors, and we compare its expression rate to that of healthy human tissues and cell cultures. Sense and antisense non-coding RNA transcripts were detected and mapped, but their secondary structure and functions remain to be elucidated. We propose that the transcripts may relate to a new class of so-called promoter-associated RNAs (pRNAs), or have some other regulatory functions. We also hope that the expression of these non-coding RNAs can be used as a marker in glioma diagnostics and prognosis.
A model of rearrangement of 32S pre-rRNA during processing was proposed. The first step of these events is the cotranscriptional interaction of the 3'-half of 5.8S rRNA and adjacent part of the internal transcribed spacer (ITS-2) with the 3'-part of the small nucleolar U3RNA from its 155th to 215th nucleotides (numbered for a rat U3RNA). This interaction prevents formation of intramolecular double-stranded structure between 5'-and 3'-end sequences of 5.8S rRNA. The second step is the appearance of extended hairpin structures in the ITS-2, which leads to a compactisation of the entire 32S-pre-rRNA molecule and to the complex formation between 5.8S rRNA and 28S rRNA sequences as the result of U3RNA displacing. After elimination of ITS-2 sequences from 32S pre-rRNA this complex can be included into ribosomes.
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