Identification of unique transcripts from a mouse full-length, subtracted inner ear cDNA library

Beisel, Kirk W.; Shiraki, Toshiyuki; Morris, Ken A.; Pompéia, Celine; Kachar, Bechara; Arakawa, Takahiro; Bono, Hidemasa; Kawai, Jun; Hayashizaki, Yoshihide; Carninci, Piero

doi:10.1016/j.ygeno.2004.01.006

Cited by 21 publications

(17 citation statements)

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“…We analyzed ESTs from publicly available normalized and/or subtracted inner ear libraries: 3,405 ESTs from a normalized fetal human cochlear library (dbEST ID.18222, Hamptonet et al 2005, unpublished), 22,576 ESTs from a subtracted cDNA library made from 7-week and older postnatal mouse inner ear (RIKEN mouse dbEST library ID.9974; Okazaki et al 2002;Beisel et al 2004), 17,468 sequence reads from a subtracted embryonic zebrafish inner ear cDNA library (dbEST Library ID.10504; Coimbra et al 2002), 1,199 EST sequences from the subtracted mouse organ of Corti library (dbEST Library ID.14415, Gerhard et al unpublished), 1,873 ESTs from a normalized library of newborn mouse inner ear transcripts (Soares NMIE dataset, dbEST Library ID.4088, Klockars et al 2003), and 20,090 ESTs from a normalized cDNA library made from rat vestibule (Wackym-Soares dataset, dbEST Library ID.16641, Roche et al 2005). Figure 1 illustrates the numbers of ion channel transcripts from the unnormalized human cochlear and mouse organ of Corti datasets.…”

Section: Cdna Libraries Genome and Ontology Resourcesmentioning

confidence: 99%

Ion Channel Gene Expression in the Inner Ear

Gabashvili

Sokolowski

Morton

et al. 2007

JARO

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The ion channel genome is still being defined despite numerous publications on the subject. The ion channel transcriptome is even more difficult to assess. Using high-throughput computational tools, we surveyed all available inner ear cDNA libraries to identify genes coding for ion channels. We mapped over 100,000 expressed sequence tags (ESTs) derived from human cochlea, mouse organ of Corti, mouse and zebrafish inner ear, and rat vestibular end organs to Homo sapiens, Mus musculus, Danio rerio, and Rattus norvegicus genomes. A survey of EST data alone reveals that at least a third of the ion channel genome is expressed in the inner ear, with highest expression occurring in hair cell-enriched mouse organ of Corti and rat vestibule. Our data and comparisons with other experimental techniques that measure gene expression show that every method has its limitations and does not per se provide a complete coverage of the inner ear ion channelome. In addition, the data show that most genes produce alternative transcripts with the same spectrum across multiple organisms, no ion channel gene variants are unique to the inner ear, and many splice variants have yet to be annotated. Our high-throughput approach offers a qualitative computational and experimental analysis of ion channel genes in inner ear cDNA collections. A lack of data and incomplete gene annotations prevent both rigorous statistical analyses and comparisons of entire ion channelomes derived from different tissues and organisms.

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Section: Cdna Libraries Genome and Ontology Resourcesmentioning

confidence: 99%

Ion Channel Gene Expression in the Inner Ear

Gabashvili

Sokolowski

Morton

et al. 2007

JARO

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“…There are, at best, only a few genes that appear to be exclusively expressed in the inner ear based on examination of the extensive EST databases, cDNA libraries, and the NCBI Gene Expression Ominbus (GEO) profiles and databases (Beisel et al, 2004). More sensitive imaging of gene expression can now be used to show all the expanded expression domains at the cellular, tissue, and temporal levels that were previously missed (Matei et al, 2005).…”

Section: Conditional Tissue-specific Inducible Systemmentioning

confidence: 99%

Conditional and inducible gene recombineering in the mouse inner ear

et al. 2006

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Genetically engineered mice have greatly improved our understanding of gene functions and disease mechanisms. Nevertheless, the traditional knock-out approach has limitations in the overall viability of mutants. The application of the Cre/loxP system in the inner ear can help bypass this difficulty by generation of conditional gene recombineering. However, to do so requires an expression system that allows ear-specific temporally inducible, gene abrogation of one or more of the increasingly available floxed genes. To date, three approaches have been successfully used to create murine inner ear-specific Cre lines: conventional transgenesis, BAC transgenesis, and gene knock-in. Unfortunately, timing of conditional Cre activity does not extend beyond the regulatory range of the gene controlling Cre expression. Rectification of this problem requires the generation of tamoxifen or tetracycline inducible systems in the inner ear. Examination of integrase expression at different loci will facilitate studies on the expression of exogenous transgenes. These genetic applications for the mouse genome will dramatically advance in vivo gene function studies. KeywordsRecombineering; Recombinase; Integrase; Transgene; Inducible; Inner ear Importance of developing recombineering mouse lines in inner earGenetically engineered mice have greatly improved our understanding of gene functions and disease mechanisms, thereby enhancing translational research Liberman et al., 2004;Zuo, 2002). While of great value, genetically engineered mice also have limitations. Such limits include embryonic lethality, leaky expression, chromosomal insertional and positional variations, strain background effects, and biological redundancy. It is demonstrated that 15-20% of germline mutations result in embryonic lethal phenotypes (Zambrowicz et al., 2003). Some of these limitations relate to the use of ubiquitous promoters to create gain-of-function (GOF) transgenic mice as well as a wider expression pattern of a gene-of-interest (GOI) or the use of a gene's endogenous promoter to examine loss-of-function (LOF) by knock-out strategies or GOF and misexpression using knock-in techniques. Much needed, more restricted expression was achieved by incorporating gene promoter cis elements into transgenic construct design using mammalian and NIH Public Access NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author Manuscript nonmammalian recombination systems. These advanced systems include noneukaryotic recombinases for excision of targeted genes, inducibility using tetracycline or tamoxifen treatments, and, most recently, transposon technology (Albanese et al., 2002;Groth and Calos, 2004;Heine et al., 2005;Izsvak and Ivics, 2004;Liu et al., 2003;Ristevski, 2005;Tian et al., 2004). Inducible switches provide experimental and therapeutic avenues for both qualitative and quantitative regulation of gene expression and manipulation of gene networks or modules. Finely controlled gene expression circuitries should increase development of successful ...

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“…Analysis of mammalian cDNA libraries derived from human fetal cochlea (Robertson et al 1994) and from rodent cochlea or organ of Corti (Ryan et al 1993;Harter et al 1999;Beisel et al 2004;Pompeia et al 2004) has identified likely cochlea-specific genes and proteins important for auditory function. Gene expression profiling with cDNA microarrays further defined the overall pattern of gene expression in the mature cochlea (Cho et al 2002) ).…”

Section: Gene Expression Profilingmentioning

confidence: 99%

Age-Related Changes in Cochlear Gene Expression In Normal and Shaker 2 Mice

Gong

Károlyi

MacDonald

et al. 2006

JARO

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The vertebrate cochlea is a complex organ optimized for sound transduction. Auditory hair cells, with their precisely arranged stereocilia bundles, transduce sound waves to electrical signals that are transmitted to the brain. Mutations in the unconventional myosin XV cause deafness in both human DFNB3 families and in shaker 2 (sh2) mice as a result of defects in stereocilia. In these mutant mice, hair cells have relatively normal spatial organization of stereocilia bundles but lack the graded, stair-step organization. We used sh2 mice as an experimental model to investigate the molecular consequences of the sh2 mutation in the Myo15 gene. Gene expression profiling with Affymetrix GeneChips in deaf homozygous (sh2/sh2) mice at 3 weeks and 3 months of age, and in age-matched, normal-hearing heterozygotes (+/sh2) identified only a few genes whose expression was affected by genotype, but a large number with age-associated changes in expression in both normal mice and sh2/sh2 homozygotes. Microarray data analyzed using Robust Multiarray Average identified Aim1, Dbi, and Tm4sf3 as genes with increased expression in sh2/sh2 homozygotes. These increases were confirmed by quantitative reverse transcription-polymerase chain reaction. Genes exhibiting altered expression with age encoded collagens and proteins involved in collagen maturation, extracellular matrix, and bone mineralization.These results identified potential cellular pathways associated with myosin XV defects, and age-associated molecular events that are likely to be involved in maturation of the cochlea and auditory function.

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Identification of unique transcripts from a mouse full-length, subtracted inner ear cDNA library

Cited by 21 publications

References 84 publications

Ion Channel Gene Expression in the Inner Ear

Ion Channel Gene Expression in the Inner Ear

Conditional and inducible gene recombineering in the mouse inner ear

Age-Related Changes in Cochlear Gene Expression In Normal and Shaker 2 Mice

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