Abstract
It has been reported that decreased Dicer expression leads to Alu RNAs accumulation in human retinal pigmented epithelium cells, and Dicer may process the endogenous SINE/B1 RNAs (the rodent equivalent of the primate Alu RNAs) into small interfering RNAs (siRNAs). In this study, we aimed to address whether Dicer can process Alu RNAs and their common ancestor, 7SL RNA. Using Solexa sequencing technology, we showed that Alu-derived small RNAs accounted for 0.6% of the total cellular small RNAs in HepG2.2.15 cells, and the abundance decreased when Dicer was knocked down. However, Alu-derived small RNAs showed different characteristics from miRNAs and siRNAs, the classic Dicer-processed products. Interestingly, we found that small RNAs derived from 7SL RNA accounted for 3.1% of the total cellular small RNAs in the control cells, and the abundance dropped about 3.4 folds in Dicer knockdown cells. Dicer-dependent biogenesis of 7SL RNA-derived small RNAs was validated by northern blotting. In vitro cleavage assay using the recombinant human Dicer protein also showed that synthetic 7SL RNA was processed by Dicer into fragments of different lengths. Further functional analysis suggested that 7SL RNA-derived small RNAs do not function like miRNAs, neither do they regulate the expression of 7SL RNA. In conclusion, the current study demonstrated that Dicer can process 7SL RNA, however, the biological significance remains to be elucidated.
Highlights
During the past 65 million years, Alu elements have evolved to more than one million copies in the primate genomes
To address whether Alu RNAs are processed by Dicer, we sequenced small RNAs extracted from Dicer knockdown and the control HepG2.2.15 cells using Solexa technology
The majority (48%) of small RNAs in the control cells were derived from annotated miRNA loci, and as expected, the fraction of miRNA was diminished to 32% in Dicer knockdown cells (Fig. 1B)
Summary
During the past 65 million years, Alu elements have evolved to more than one million copies in the primate genomes. The typical Alu element is ,300 base pairs long and exhibits a dimeric structure, which is separated by an A-rich linker region. It contains an internal RNA polymerase III (Pol III) promoter (A and B boxes) at the 59 region and ends with an oligo dA-rich tail of variable length [1]. Being considered by some scientists as an example of ‘‘junk DNA’’, Alu elements do play important roles. They affect the genome in several ways, causing insertion mutations, DNA recombination, gene conversion and altered gene transcription [1,2]. Alu RNAs play major roles in post transcriptional regulation of gene expression, by affecting protein translation, alternative splicing and mRNA stability [3]
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