microRNAs |
19–22 nt long; pri-miRNAs are transcribed by RNA pol II from single or multi cistronic units. The primary transcript is then processed into a hairpin like structure by Drosha. Maturation of pre-miRNA into mature microRNAs occurs in the cytoplasm and is mediated by DICER1, which cleave the 70 nt long pri-miR into 20–22 nt long RNAs molecules. These short RNAs are then loaded into Argonaute proteins 1–4 (AGO1–4) and the complex then associates with its mRNA target(s). |
Inhibition of mRNA translation or stability by base pairing with complementary seed sequence in 3UTR of target mRNAs. microRNAs can mediate almost any biological function (from cell proliferation to cell death, from oncogenic transformation to tumor suppression) depending on their targets. |
4, 5, 10
|
Long non-coding RNAs |
Long non-coding RNAs (lncRNAs) are generally defined as RNA transcripts longer than 200 bp. They share features with protein coding genes including poliA tail, 5’capping, association with rybosomes. They can be transcribed in both orientations (sense and antisense), from intergenic regions (lncRNAs) overlapping with coding genes, from repetitive sequence within telomeres or from introns. Some encode for small peptides, usually no longer than few hundred aminoacid. |
Molecularly, lncRNAs mediate a wide range of functions both in-cis and in-trans including chromatin remodelling, genomic imprinting, regulation of transcription regulation of RNA processing, stability and splicing. lncRNAs can also function as molecular decoy for proteins or sponges for other transcripts. |
6, 7, 10
|
Circular RNAs |
Circular RNAs (circRNAs) are generated through non-canonical splicing events involving non- juxtaposed exons, head to tail splicing of the same exon, and intronic RNAs. Non-canonical splicing of exonic circRNAs is favored by the presence of repeated Alu sequences flanking the spliced exons. |
Compared to other classes of non-coding genes, there are fewer examples of functional circRNAs. circRNAs have been shown to function as microRNAs sponges and to modulate protein functions. |
12–16
|
Pseudogenes |
Pseudogenes are copies of their corresponding parental genes that have lost their ability to code for proteins. Depending on their biogenesis, there are three distinct classes of pseudogenes: unitary, processed and transcribed. |
Pseudogenes mainly regulate their parental gene expression. Examples include: competition for microRNA binding sites, regulation of their parental mRNA stability, crosstalk with the RNAi pathway and modulation of the epigenetic status of parental genes. |
17–20
|
snoRNAs |
Small nucleolar RNAs (snoRNAs) are divided into two classes: box C/D snoRNAs and box H/ACA snoRNAs. They are 70–120 bp long and have complex secondary structures. |
snoRSNAs mediate ribosomal RNAs (rRNAs) modifications. Box C/D RNAs mediate 2′-O-methylation, while box H/ACA family of snoRNAs guide pseudouridylation or rRNA. |
8,9
|
piwiRNAs |
PIWI-interacting RNAs or piRNAs are a class of short RNAs (26–31nt long) that are associated with PIWI proteins. They are mainly found in germline cells in both male and females. |
They safeguard genomic stability in germline cells. They have been shown to bind to and mediate the silencing of transposable elements post-transcriptionally. Loss of piRNAs or PIWI proteins has the most severe defects in male germline cells. PIWI deficient cells show fertility defects. |
43 |
tRNAs |
tRNAs are the most abundant class of RNAs within the cell. tRNAs are essential constituents of the translational machinery and they function to transport amino acids to the ribosome for the translation of mRNAs into polypeptide chains. Each tRNA is modified at its tail to carry one specific amino acid. The binding between tRNAs and mRNAs involves codon/anticodon pairing. |
Recent findings show that tRNAs can also function as regulatory molecules. Distinct classes of tRNAs have been implicated in cancer metastasis. Several mitochondrial diseases including myopathies and encephalopathies, have mutation in mt- tRNAs. Human diseases associated with mutations in enzymes involved in tRNA biogenesis include neurological disease, metabolic syndromes and cancer. |
5, 85–89 |