Heat shock increases lifetime of a small RNA and induces its accumulation in cells

• Published in: Gene 2016-08, Vol.587 (1), p.33-41
• Main Authors: Tatosyan, Karina A., Kramerov, Dmitri A.
• Format: Article
• Language: English
• Subjects: Animals; Cardiovirus Infections - metabolism; Cell Line; Cell Line, Tumor; Cells, Cultured; Encephalomyocarditis virus; Encephalomyocarditis virus - physiology; Heat shock; Mice; Muridae; Non-coding RNA; Rats; RNA decay; RNA Stability; RNA turnover; RNA, Small Interfering - genetics; RNA, Small Interfering - metabolism; Rodents; Stress, Physiological; Transcription, Genetic
• ISSN: 0378-1119; 1879-0038
• DOI: 10.1016/j.gene.2016.04.025

4.5SH and 4.5SI RNA are two abundant small non-coding RNAs specific for several related rodent families including Muridae. These RNAs have a number of common characteristics such as the short length (about 100nt), transcription by RNA polymerase III, and origin from Short Interspersed Elements (SINEs). However, their stabilities in cells substantially differ: the half-life of 4.5SH RNA is about 20min, while that of 4.5SI RNA is 22h. Here we studied the influence of cell stress such as heat shock or viral infection on these two RNAs. We found that the level of 4.5SI RNA did not change in stressed cells; whereas heat shock increased the abundance of 4.5SH RNA 3.2–10.5 times in different cell lines; and viral infection, 5 times. Due to the significant difference in the turnover rates of these two RNAs, a similar activation of their transcription by heat shock increases the level of the short-lived 4.5SH RNA and has minor effect on the level of the long-lived 4.5SI RNA. In addition, the accumulation of 4.5SH RNA results not only from the induction of its transcription but also from a substantial retardation of its decay. To our knowledge, it is the first example of a short-lived non-coding RNA whose elongated lifetime contributes significantly to its accumulation in stressed cells. •Heat shock causes significant increase in the level of 4.5SH RNA in rodent cells.•Retardation of 4.5SH RNA decay contributes to this phenomenon.•Activation of 4.5SH RNA synthesis also leads to its accumulation in stressed cell.•4.5SH RNA level and stability increase during viral infection of cells.