mir-155


mir-155
mir-155
MiR-155 secondary structure.png
miR-155 secondary structure and sequence conservation.
Identifiers
Symbol mir-155
Rfam RF00731
miRBase family MIPF0000157
Other data
RNA type microRNA
Domain(s) Eukaryota;

MicroRNAs are non-coding RNAs (ncRNAs) that regulate the expression levels of other genes through several mechanisms at a post transcriptional stage, they work by inactivating translation of gene or gene clusters or by degrading genes. About 30 percent of the eukaryotic genome is controlled by miRNAs, the estimated total number of miR genes is ~1000.[citation needed] They exert influences on cellular processes of proliferation, differentiation, apoptosis and metabolism.[1] [2] [3]

One such showcase of this multi-activity is displayed by the microRNA mir-155, a short RNA molecule that plays a crucial role in various physiological and pathological processes. Potentially, exogenous molecular control in vivo of miR-155 expression could uncover new frontiers to restrain malignant growth and viral infections, or to attenuate the progression of cardiovascular diseases for instance.

Contents

Phylogenetic Characteristics:

MiRNAs are phylogentically diverse, some miRNAs are more restricted to single species, some are present throughout different cell types, some have isoforms and others have only single forms. With regard to miR-155, its distribution across the animal kingdom shows very well conservation throughout, it was identified in a wide range of species controlling many key processes by having a target on many genes that are implicated in various levels of cell regulation and proliferation [2][3]. In fact, its overexpression or underexression has been found to guide many processes that involve immunity, inflammation, cancer...etc.miR-155 is also expressed in mammalian reproductive tissues, fibroblasts, epithelial tissues, and the central nervous system.

Searching MiRBase for 'Mir-155' -as of October, 2011- has retrieved records for 17 organisms that contain miR-155 in various genomic locations; in the mouse, the miR-155 on Chromosome 16 B-cell Integration Cluster (BiC) region shares very close homology to that in humans, with the mature region of the miRNA that is responsible for its gene-silencing effect being of high conservation.

MiR-155 Biogenesis:

On the human genome, miR-155 gene is about 1500 bases long located on the BiC area on chromosome 21 band q21.3. Transcription in this areas releases a non-coding RNA product that upon processing finalization becomes miR-155. This particular chromosomal location shows strong sequence conservation in humans, mouse, chicken and explains the distinct expression profiles for miR-155 seen across many species[2]. In the UCSC browser the entry name for this gene is MIR155HG. The NCBI nucleotide database saves pertinent information on this gene under record number NR_001458.

Manufacturing miR-155 starts in the nucleus and ends in the cytoplasm navigating through many post-transcriptional processing that transforms its nascent initial hairpin-fold-like double-stranded structure into the single-stranded silencer that it is[4] . The sequence of events that culminate into building an active silencing machinery based on miR-155 is summarized as follows:

  • MiR genes are transcribed into pri-miRNAs via RNA polymerase II in the nucleus.
  • Pri-miRNAs are processed into pre-miRNAs via Drosha and DGCR8.
  • Pre-miRNA leaves the nucleus into the cytoplasm carried by the enzyme exportin.
  • In the cytoplasm, pre-miRNA is cleaved by the endonuclease Dicer resulting in a duplex RNA that has a guide strand and a passenger strand (the later usually degraded).
  • The mature guide strand is loaded into the RNA-Induced Silencing Complex RISC.
  • Upon this integration RISC becomes activated.

This complex process involves orchestrated interplay of proteins and cofactors, it begins in transcription by polymerases, export to the cytoplasm by exportin, endonuclease splicing by Dicer where the originally double-stranded miR-155 precursor is spliced into smaller (21-23 nucleotides) single stranded RNAs, and finally, processing and complexing with RISC [2]. The sequence of the RNA latched onto the RISC complex guides it to its target gene-transcript mRNA by virtue of complementarity, upon reaching there; RISC attaches to, cleaves and neutralizes that target[3]. This silencing effect is brought about by either repressing the translation of that gene or degrading the target mRNA depending on whether the complementarity is partial or perfect.

The pathways that involve biogenesis and Dicer splicing are conserved in animals, plants and fungi; however, silencing mechanisms may differ between plants and animals. In plants, miRNAs action mimics the exogenously introduced siRNAs, they flag their target mRNAs for silencing by endonucleolytic cleavage whereas in animals, silencing is brought about by translational repression. In addition, complementarity between animals miRNAs and their targets is not a must for miRNAs activity since partial complementarity is enough to bring about silencing; a scenario contrary to what happens in plants miRNAs. On the other hand, Yeast have a silencing complex similar to RISC called (RNA-induced initiation of transcriptional gene silencing) RITS[3].

MiR-155 Activity and Phenotypes:

The hallmark of miR-155 activities is that they transcend to and fro within protective roles to normal physiological functions to disease associated manifestations. It is estimated to participate in cascades associated with cardiovascular diseases and hypertension, and was also found to be implicated in immunity, genomic instability, cell differentiation, inflammation, virus associated infections and cancer.

Mode of Action:

Protective roles of miR-155 may arise in response to its action on silencing genes thereby regulating their expression time, mutations in miR-155 target site deny it the optimal access necessary to bring about gene silencing, leading to over abundance of delinquent activities that may go malignant, for example, miR-155 role as a protective agent against predisposition to B Cell associated malignancies is emphasized by maintaining the balance of Activation-Induced Cytidine Deaminase (AID) enzyme. MiR-155 mediates regulation of AID abundance and expression time upon immunological cues however, mutations in the target on AID mRNA result in its unresponsiveness to miR-155 silencing and lead to unbridled expression of its protein causing wild immature B-lymphocyte surges and AID-mediated chromosomal translocations[3][4].

Cardiopulmonary Disease and Hypertension:

Transfection of miR-155 into human primary lung fibroblasts reduces the endogenous expression of the angiotensin II receptor AT1R protein. Furthermore, AT1R is involved in cardiovascular and blood pressure ailments by controlling angiotension II. Defective miR-155 function could be implicated in hypertension and cardiovascular diseases if the cis-regulatory site on 3` UTR of AT1R (miR-155 target site) was affected due to a SNP polymorphism in AT1R itself. This mutation is disruptive of miR-155 targeting and thus preventive of AT1R expression down-regulation [3]. In low blood pressure over-expression of miR-155 correlates with the impairment of AT1R activity.[2]

Immunity:

miR-155 is highly involved in immunity by playing key roles in modulating humoral and innate cell-mediated immune responses, for example, In miR-155 deficient mice, immunological-memory is impaired; making it fall prey to repetitive bouts of invasions by the same pathogen (Rodriguez et al. 2007),maturation and specificity of miR-155-deficient B-lymphocytes are impaired since the process relies on AID enzyme which has a miR-155 target in its 3' UTR end [3][4]. The phenotypic consequences involving deficiency of miR-155 in mice show later in life where the animals develop lung and intestinal lesions. [2]

Activated B and T cells show increased miR-155 expression, the same goes for macrophages and dendritic cells of the immune system. MiR-155 is crucial for proper lymphocyte development and maturation. Details of various manifestations of miR-155 levels and involvement in activities that ascertain optimal immune responses have been the subject of many researches:

Reduction of IgG1:

Defective T and B cells as well as markedly decreased IgG1 responses were observed in miR-155-deficient mice, IgG1 is reduced whereas the expression of the IgM immunoglobulin remains normal in these mice. The abnormality in IgG1 levels maybe explained by an important target for miR-155 in B cells, the protein-encoding mRNA for the transcriptional regulator Pu.1-protein, elevation of Pu.1 protein predisposes defective IgG1 production. In addition to Pu.1, there are nearly 60 other differentially elevated genes in miR-155 deficient B cells, further inspection revealed possible miR-155 target sites in the 3' UTR regions in these genes [4].

Predisposition to Lymphocyte Malignancies:

Mature receptors affinity and specificity of lymphocytes to pathogenic agents underly proper immune responses, optimal miR-155 coordination is required for manufacturing of normal B lymphocytes and production of high-affinity antibodies and memory cells, this has been evidenced by comparisons of miR-155 expression patterns in normal and abnormal B cells revealing a miR-155 role in differentiation. Were miR-155 expression abnormally elevated; pre-B cell lymphomas formed [4]. By Understanding how the process of B cell development takes place we can clearly see the significance of miR-155 in this regard; selection of competent B cells takes place in the germinal center where they are trained to differentiate body cells vs. foreign antigens, they compete for antigen recognition and for T cell help, in this fashion of selective pressure those B Cells that demonstrated high-affinity receptors and cooperation with T cells (affinity maturation) are recruited and deployed to the bone marrow or become memory B cells,apoptotic termination takes place for those B Cells failing the competition. Immature B cells which are miR-155 deficient evade apoptosis as a result of elevated Bcl-2 protein levels; a protein that was found to be involved in B Cell malignancies and to be controlled by miR-155[4].

Inflammation:

Inflammatory responses to triggers such as TNF-α involve macrophages with components that include miR-155. In Autoimmune disorders such as Rheumatoid Arthritis miR-155 showed higher expression in patients' tissues and synovial fibroblasts. [2]

DNA Viruses:

In DNA viruses, miRNAs were experimentally verified, miRNAs in viruses are encoded by dsDNAs [3], examples of such viruses include herpesviruses such as Humans-Epstein-Barr Virus (EBV) and adenoviruses [2], another virus expressing miR-155-like miRNA in chickens is the oncogenic MDV-1 whose non-oncogenic relative MDV-2 does not, this suggests implication of miR-155 in lymphomagenesis[3]. Viruses can exploit host miRNAs to the degree that they use host miRNAs to encode for viral clones for example: MiR-k12-11 in Kaposi's-sarcoma-associated Herpesvirus has a target specificity region orthologous to that of miR-155's; mimicking the action of miR-155 [2][3] and, sharing targets with it, thus it can be thought to suppress miR-155 accessibility to its targets by competition and this in effect downregulates expression of genes playing roles in cellular growth and apoptosis in a manner that defies regulations by miR-155[2]. EBV modulates host miR-155. EBV-infected cells have increased expression of miR-155 thereby disturbing equilibrium of expression for genes regulating transcription in those cells[3][2].

Cancer:

Over-silencing by miR-155 may result in triggering oncogenic cascades that begin by apoptotic resistance, The pro-apoptotic Tumour Protein-53-induced-nuclear-protein1 (TP53INP1) is silenced by miR-155, over-expression of miR-155 leads to decreased levels of TP53INP1 in pancreatic ductal adenocarcinomas and possibly in other epithelial cancers where TP53INP1 activity is lost thereby resulting in apoptosis evasion and uncontrolled bouts of growth[3].

Inactivation of DNA Mismatch Repair (MMR) as identified by elevation of mutation rates is the cause of Lynch Syndrome ((LS), also known as hereditary nonpolyposis colorectal cancer (HNPCC), down-regulation of MMR controlling protein is carried out by over-expression of miR-155, MMR is controlled by a group of highly conserved proteins, reduced activity of these proteins results in elevated levels of mutations in the phenotype triggering a march towards developing this type of cancer [1].

Other types of tumors in which miR-155 over-expression was reported include: thyroid carcinoma, breast cancer, colon cancer, cervical cancer, and lung cancer, where distinct miR-155 expression profiles quantification can potentially serve as signals for tumor detection and evaluation of prognosis outcome[2].

Targets:

On the transcripts level, microRNAs affect replication, translation and stability of genes by interacting with the riboswitches and cis-regulatory sites of these transcripts. These control elements are typically located in the untranslated regions UTRs on either ends of the transcript and their interactions with microRNAs regulate the activity of their gene expression. However, the target sequences for miRNAs in animals are mainly present in the 3' UTR end of the mRNAs.

So far, MiR-155 targets are estimated to number into 991, however, it is worth noting that not all in silico predicted targets have been found to be responsive to the miRNA control upon experimental validation[2]., the existence for many targets per miRNA on mRNA transcripts can also be explained by the various levels of complementarity between the target sequences and the miRNA sequence itself thereby explaining different degrees of silencing efficiency exerted by miRNA influence on each one of its targets. MiR-155 targets involve members falling into many categories:

  • Transcriptional Regulatory Genes
  • Protein Receptors
  • Nuclear Proteins
  • Binding Proteins

This underscores the variety of roles miR-155 plays in transcripts control and cellular processes by interacting with the 3'UTR regions in these genes[2].

Images

Further reading

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