A role for epigenetics in hearing: Establishment and maintenance of auditory specific gene expression patterns

Provenzano, Matthew J.; Domann, Frederick E.

doi:10.1016/j.heares.2007.07.002

Cited by 38 publications

(25 citation statements)

References 120 publications

(130 reference statements)

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“…While over 100 loci have been mapped and 44 protein-coding genes with mutations have been cloned (Hereditary Hearing Loss Homepage; http://webh01.ua.ac.be/hhh/), many cases of hereditary hearing loss remain a mystery. Approximately 98% of RNAs in mammalian cells do not code for proteins and epigenetic factors are associated with hearing loss (4), raising the possibility that noncoding RNAs, such as microRNAs (miRNAs), may also be involved in inner ear development and hearing loss. miRNAs are 17 to 25 nt RNAs produced from stem-loop precursors (pre-miRNAs) that are encoded by miR genes (also known as Mirn genes).…”

mentioning

confidence: 99%

MicroRNAs are essential for development and function of inner ear hair cells in vertebrates

Friedman¹,

Dror²,

Mor³

et al. 2009

Proc. Natl. Acad. Sci. U.S.A.

166

188

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MicroRNAs (miRNAs) inhibit the translation of target mRNAs and affect, directly or indirectly, the expression of a large portion of the protein-coding genes. This study focuses on miRNAs that are expressed in the mouse cochlea and vestibule, the 2 inner ear compartments. A conditional knock-out mouse for Dicer1 demonstrated that miRNAs are crucial for postnatal survival of functional hair cells of the inner ear. We identified miRNAs that have a role in the vertebrate developing inner ear by combining miRNA transcriptome analysis, spatial and temporal expression patterns, and bioinformatics. Microarrays revealed similar miRNA profiles in newborn-mouse whole cochleae and vestibules, but different temporal and spatial expression patterns of six miRNAs (miR-15a, miR-18a, miR-30b, miR-99a, miR-182, and miR-199a) may reflect their roles. Two of these miRNAs, miR-15a-1 and miR-18a, were also shown to be crucial for zebrafish inner ear development and morphogenesis. To suggest putative target mRNAs whose translation may be inhibited by selected miRNAs, we combined bioinformatics-based predictions and mRNA expression data. Finally, we present indirect evidence that Slc12a2, Cldn12, and Bdnf mRNAs may be targets for miR-15a. Our data support the hypothesis that inner ear tissue differentiation and maintenance are regulated and controlled by conserved sets of cell-specific miRNAs in both mouse and zebrafish.cochlea ͉ deafness ͉ Dicer ͉ mouse ͉ zebrafish

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mentioning

confidence: 99%

MicroRNAs are essential for development and function of inner ear hair cells in vertebrates

Friedman¹,

Dror²,

Mor³

et al. 2009

Proc. Natl. Acad. Sci. U.S.A.

166

188

View full text Add to dashboard Cite

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“…Interestingly, alterations in DNA methylation have also been associated with several syndromes that cause hearing related problems (Provenzano and Domann, 2007). For instance DNA hypomethylation has been related with hearing loss in patients with ICF syndrome (immunodeficiency, centromere instability, facial anomalies) (Robertson et al, 1999; Xie et al, 1999).…”

Section: Discussionmentioning

confidence: 99%

The epigenetic modifier DNMT3A is necessary for proper otic placode formation

Roellig

Bronner‐Fraser

2016

Developmental Biology

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Cranial placodes are thickenings in the ectoderm that give rise to sensory organs and peripheral ganglia of the vertebrate head. At gastrula and neurula stages, placodal precursors are intermingled in the neural plate border with future neural and neural crest cells. Here, we show that the epigenetic modifier, DNA methyl transferase (DNMT) 3A, expressed in the neural plate border region, influences development of the otic placode which will contribute to the ear. DNMT3A is expressed in the presumptive otic region at gastrula through neurula stages and later in the otic placode itself. Whereas neural plate border and non-neural ectoderm markers Erni, Dlx5, Msx1 and Six1 are unaltered, DNMT3A loss of function leads to early reduction in the expression of the key otic placode specifier genes Pax2 and Gbx2 and later otic markers Sox10 and Soho1. Reduction of Gbx2 was first observed at HH7, well before loss of other otic markers. Later, this translates to significant reduction in the size of the otic vesicle. Based on these results, we propose that DNMT3A is important for enabling the activation of Gbx2 expression, necessary for normal development of the inner ear.

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“…To date, more than 100 gene loci have been demonstrated to be involved in deafness, 44 of which have been reported to possess at least on mutation; however, there are still a large number of unexplained cases. Approximately 98% of RNA in mammalian cells do not code protein [7] and non-coding RNA such as miRNAs may be involved in the development of the inner ear and thus have a role in hearing loss [8]. In 2005 miRNAs were identified in the vestibular system for the first time.…”

Section: History Of Mirna and Biogenesismentioning

confidence: 99%

MicroRNA-183 Family in Inner Ear: Hair Cell Development and Deafness

sani

Hashemzadeh‐Chaleshtori

Saidijam

et al. 2016

J Audiol Otol

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miRNAs are essential factors of an extensively conserved post-transcriptional process controlling gene expression at mRNA level. Varoius biological processes such as growth and differentiation are regulated by miRNAs. Web of Science and PubMed databases were searched using the Endnote software for the publications about the role miRNA-183 family in inner ear: hair cell development and deafness published from 2000 to 2016. A triplet of these miRNAs particularly the miR-183 family is highly expressed in vertebrate hair cells, as with some of the peripheral neurosensory cells. Point mutations in one member of this family, miR-96, underlie DFNA50 autosomal deafness in humans and lead to abnormal hair cell development and survival in mice. In zebrafish, overexpression of the miR-183 family induces extra and ectopic hair cells, while knockdown decreases the number of hair cell. The miR-183 family (miR-183, miR-96 and miR-182) is expressed abundantly in some types of sensory cell in the eye, nose and inner ear. In the inner ear, mechanosensory hair cells have a robust expression level. Despite much similarity of these miRs sequences, small differences lead to distinct targeting of messenger RNAs targets. In the near future, miRNAs are likely to be explored as potential therapeutic agents to repair or regenerate hair cells, cell reprogramming and regenerative medicine applications in animal models because they can simultaneously down-regulate dozens or even hundreds of transcripts.

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A role for epigenetics in hearing: Establishment and maintenance of auditory specific gene expression patterns

Cited by 38 publications

References 120 publications

MicroRNAs are essential for development and function of inner ear hair cells in vertebrates

MicroRNAs are essential for development and function of inner ear hair cells in vertebrates

The epigenetic modifier DNMT3A is necessary for proper otic placode formation

MicroRNA-183 Family in Inner Ear: Hair Cell Development and Deafness

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