Differences in vertebrate microRNA expression

Ason, Brandon; Darnell, Diana K.; Wittbrodt, Joachim; Berezikov, Eugène; Kloosterman, Wigard P.; Wittbrodt, Jochen; Antin, Parker B.; Plasterk, Ronald H.A.

doi:10.1073/pnas.0603529103

Cited by 234 publications

(200 citation statements)

References 35 publications

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“…Skeletal precursors across vertebrate species express mirn140 [21][22][23][24] and mirn140 occupies the orthologous intron in wwp2 of zebrafish, human, and other vertebrates ( Supplementary Fig. 1), prompting the hypothesis that Mirn140 plays a conserved role in skeletogenesis across vertebrate species.…”

Section: Mirn140 and Pdgf Signaling Regulate Palatal Development In Zmentioning

confidence: 99%

“…Most Pdgfc mutants have cleft palate 15 MicroRNAs (miRNAs) provide a unique mechanism for modulating signaling pathways [17][18][19][20] . Skeletogenic, including palatal, precursors express mirn140 (miR-140) in teleosts 21 and amniotes [22][23][24] , suggesting that Mirn140 may modulate signaling during palatogenesis across vertebrate species. Despite the function of miRNAs in development and the importance of neural crest in evolution and disease, no miRNA has yet been shown to regulate neural crest development or cellular behaviors.…”

Section: Introductionmentioning

confidence: 99%

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MicroRNA Mirn140 modulates Pdgf signaling during palatogenesis

et al. 2008

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Disruption of signaling pathways such as those mediated by Shh or Pdgf causes craniofacial disease, including cleft palate. The role that microRNAs play in modulating palatogenesis, however, is completely unknown. We show, in zebrafish, that the microRNA Mirn140 negatively regulates Pdgf signaling during palatal development and we provide a mechanism for how disruption of Pdgf signaling causes palatal clefting. The pdgf-receptor alpha (pdgfra) 3' UTR contains a Mirn140 binding site functioning in the negative regulation of Pdgfra protein levels in vivo. Both pdgfra mutants and Mirn140-injected embryos share panoply of facial defects including clefting of the crestderived cartilages that develop in the roof of the larval mouth. Concomitantly, the oral ectoderm beneath where these cartilages develop loses pitx2 and shha expression. Mirn140 modulates Pdgfmediated attraction of cranial neural crest cells to the oral ectoderm, where crest-derived signals are necessary for oral ectodermal gene expression. Both Mirn140 loss-of-function and pdgfra overexpression alters palatal shape and causes neural crest cells to accumulate around the optic stalk, a source of the ligand Pdgfaa. Conserved molecular genetics and expression patterns of mirn140 and pdgfra suggest that their regulatory interactions are ancient methods of palatogenesis that provide a candidate mechanism for cleft palate.Cleft palate and other craniofacial diseases are common in humans and have complex cellular and genetic etiologies. In amniotes, the palate serves to separate the nasal and oral cavities and is generated through an intricate series of morphogenic events that include early neural crest cell migration and cell-cell signaling during the formation of facial prominences, as well as later generation and fusion of palatal shelves. While later events involving palatal shelves have not been described in zebrafish, palatal precursors migrate both rostral and caudal to the eye to condense upon the oral ectoderm in amniotes 1 as well as zebrafish 2,3 and evidence continues to accumulate that the early signaling environment governing palatogenesis is also largely equivalent [3][4][5][6] . For instance, Hh signaling is crucial for palatogenesis in humans and zebrafish 3,4,7 . Zebrafish and amniotes also share expression patterns of palatogenic genes such as Shh 4,8 , Fgf8 4,9,10 and Pdgf receptor alpha (Pdgfra) [11][12][13] .In mouse, the Pdgf family consists of four soluble ligands, Pdgfa, Pdgfb, Pdgfc, and Pdgfd as well as two receptor tyrosine kinases, Pdgfra and Pdgfrb 14 . Pdgf signaling regulates a myriad of biological processes as demonstrated by analyses of mouse Pdgf ligand and receptor mutants 14 . Mice null for Pdgfra have a facial clefting phenotype that includes cleft palate 12,13 . This facial phenotype is fully recapitulated in mice doubly mutant for Pdgfa and Pdgfc 15. Most Pdgfc mutants have cleft palate 15 MicroRNAs (miRNAs) provide a unique mechanism for modulating signaling pathways [17][18][19][20] . Skeletogenic, including...

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Section: Mirn140 and Pdgf Signaling Regulate Palatal Development In Zmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

MicroRNA Mirn140 modulates Pdgf signaling during palatogenesis

et al. 2008

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“…Recent advances have shown that miRNA expression during development is highly tissue-specific (9)(10)(11)(12), which suggests that miRNA may be involved in specifying and maintaining tissue identity. For example, the expression of miR-124a is restricted to the brain and spinal cord in the fish and the mouse, and to the ventral nerve cord in the fly (13).…”

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confidence: 99%

MicroRNA‐124a is a key regulator of proliferation and monocyte chemoattractant protein 1 secretion in fibroblast‐like synoviocytes from patients with rheumatoid arthritis

Nakamachi¹,

Kawano²,

Takenokuchi³

et al. 2009

Arthritis & Rheumatism

302

209

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Objective. To elucidate the role of microRNA (miRNA) in the pathogenesis of rheumatoid arthritis (RA), we analyzed synoviocytes from RA patients for their miRNA expression.Methods. Synoviocytes derived from surgical specimens obtained from RA patients were compared with those obtained from osteoarthritis (OA) patients for their expression of a panel of 156 miRNA with quantitative stem-loop reverse transcription-polymerase chain reaction. The miRNA whose expression decreased or increased in RA synoviocytes as compared with OA synoviocytes were identified, and their target genes were predicted by computer analysis. We used an in vitro system of enhancing the expression of specific miRNA by transfection of precursors into synoviocytes, and then we performed proliferation, cell cycle, and apoptosis assays, as well as enzyme-linked immunosorbent assays for cytokine production. The effects of transfection on predicted target protein and messenger RNA (mRNA) were then examined by Western blot analysis and luciferase reporter assay.Results. We found that miR-124a levels significantly decreased in RA synoviocytes as compared with OA synoviocytes. Transfection of precursor miR-124a into RA synoviocytes significantly suppressed their proliferation and arrested the cell cycle at the G 1 phase. We identified a putative consensus site for miR-124a binding in the 3 -untranslated region of cyclin-dependent kinase 2 (CDK-2) and monocyte chemoattractant protein 1 (MCP-1) mRNA. Induction of miR-124a in RA synoviocytes significantly suppressed the production of the CDK-2 and MCP-1 proteins. Luciferase reporter assay demonstrated that miR-124a specifically suppressed the reporter activity driven by the 3 -untranslated regions of CDK-2 and MCP-1 mRNA.Conclusion. The results of this study suggest that miR-124a is a key miRNA in the posttranscriptional regulatory mechanisms of RA synoviocytes.MicroRNA (miRNA) are a well-established class of small (ϳ22 nucleotides) endogenous noncoding RNAs that influence the stability and translation of messenger RNA (mRNA) (1). Using various computational and experimental approaches, hundreds of miRNA have been identified in numerous animal species. The miRNA genes are transcribed by RNA polymerase II as primary miRNA (pri-miRNA) (2,3). The RNase III enzyme Drosha then processes the nuclear pri-miRNA, yielding a ϳ70-nucleotide molecule known as precursor miRNA (pre-miRNA) (4), which is exported from the nucleus. Maturation of the pre-miRNA into miRNA is then mediated by the cytoplasmic enzyme Dicer (5), after which the mature miRNA is loaded into the RNA-induced silencing complex (RISC)

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“…Plasterk and colleagues have used an ISH method based on Locked Nucleic Acid (LNA) oligonucleotide probes to detect mature miRNAs in whole mounts of zebrafish and mouse embryos [ 11,12 ]. The LNAbased ISH methodology has been applied to whole-mount embryos from a variety of vertebrate species, including chicken and medaka [ 13,14 ], and for the analysis of adult human brain sections [ 15 ] as well as mouse tissue sections [ 16,17 ]. Independently, we have developed a miRNA ISH method based upon RNA oligonucleotide probes and have used this method for the detection of mature miRNAs in tissue sections from embryonic and adult mice [ 18 ], as well as from rat and human brains (this article) and zebrafish (our unpublished observations).…”

Section: Introductionmentioning

confidence: 99%

Analysis of microRNA expression by in situ hybridization with RNA oligonucleotide probes

Thompson

Deo

Turner

2007

Methods

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In situ hybridization is an important tool for analyzing gene expression and developing hypotheses about gene functions. The discovery of hundreds of microRNA (miRNA) genes in animals has provided new challenges for analyzing gene expression and functions. The small size of the mature miRNAs (∼20-24 nucleotides in length) presents difficulties for conventional in situ hybridization methods. However, we have developed a modified in situ hybridization method for detection of mammalian miRNAs in tissue sections, based upon the use of RNA oligonucleotide probes in combination with highly specific wash conditions. Here we present detailed procedures for detection of miRNAs in tissue sections or cultured cells. The methods described can utilize either nonradioactive hapten-conjugated probes that are detected by enzyme-coupled antibodies, or radioactively labeled probes that are detected by autoradiography. The ability to visualize miRNA expression patterns in tissue sections provides an additional tool for the analyses of miRNA expression and function. In addition, the use of radioactively labeled probes should facilitate quantitative analyses of changes in miRNA gene expression.

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Differences in vertebrate microRNA expression

Cited by 234 publications

References 35 publications

MicroRNA Mirn140 modulates Pdgf signaling during palatogenesis

MicroRNA Mirn140 modulates Pdgf signaling during palatogenesis

MicroRNA‐124a is a key regulator of proliferation and monocyte chemoattractant protein 1 secretion in fibroblast‐like synoviocytes from patients with rheumatoid arthritis

Analysis of microRNA expression by in situ hybridization with RNA oligonucleotide probes

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