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  • 1
    Online Resource
    Online Resource
    5′-Transducing SVA retrotransposon groups spread efficiently throughout the human genome
    Cold Spring Harbor Laboratory ; 2009
    In:  Genome Research Vol. 19, No. 11 ( 2009-11), p. 1992-2008
    Details
    In: Genome Research, Cold Spring Harbor Laboratory, Vol. 19, No. 11 ( 2009-11), p. 1992-2008
    Abstract: SVA elements represent the youngest family of hominid non-LTR retrotransposons, which alter the human genome continuously. They stand out due to their organization as composite repetitive elements. To draw conclusions on the assembly process that led to the current organization of SVA elements and on their transcriptional regulation, we initiated our study by assessing differences in structures of the 116 SVA elements located on human chromosome 19. We classified SVA elements into seven structural variants, including novel variants like 3′-truncated elements and elements with 5′-flanking sequence transductions. We established a genome-wide inventory of 5′-transduced SVA elements encompassing ∼8% of all human SVA elements. The diversity of 5′ transduction events found indicates transcriptional control of their SVA source elements by a multitude of external cellular promoters in germ cells in the course of their evolution and suggests that SVA elements might be capable of acquiring 5′ promoter sequences. Our data indicate that SVA-mediated 5′ transduction events involve alternative RNA splicing at cryptic splice sites. We analyzed one remarkably successful human-specific SVA 5′ transduction group in detail because it includes at least 32% of all SVA subfamily F members. An ancient retrotransposition event brought an SVA insertion under transcriptional control of the MAST2 gene promoter, giving rise to the primal source element of this group. Members of this group are currently transcribed. Here we show that SVA-mediated 5′ transduction events lead to structural diversity of SVA elements and represent a novel source of genomic rearrangements contributing to genomic diversity.
    Type of Medium: Online Resource
    ISSN: 1088-9051
    URL: Article
    DOI: 10.1101/gr.093435.109
    RVK:
    XA 10000
    Language: English
    Publisher: Cold Spring Harbor Laboratory
    Publication Date: 2009
    detail.hit.zdb_id: 1483456-X
    SSG: 12
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  • 2
    Online Resource
    Online Resource
    Analysis of 5′ junctions of human LINE-1 and Alu retrotransposons suggests an alternative model for 5′-end attachment requiring microhomology-mediated end-joining
    Cold Spring Harbor Laboratory ; 2005
    In:  Genome Research Vol. 15, No. 6 ( 2005-06), p. 780-789
    Details
    In: Genome Research, Cold Spring Harbor Laboratory, Vol. 15, No. 6 ( 2005-06), p. 780-789
    Abstract: Insertion of the human non-LTR retrotransposon LINE-1 (L1) into chromosomal DNA is thought to be initiated by a mechanism called target-primed reverse transcription (TPRT). This mechanism readily accounts for the attachment of the 3′-end of an L1 copy to the genomic target, but the subsequent integration steps leading to the attachment of the 5′-end to the chromosomal DNA are still cause for speculation. By applying bioinformatics to analyze the 5′ junctions of recent L1 insertions in the human genome, we provide evidence that L1 uses at least two distinct mechanisms to link the 5′-end of the nascent L1 copy to its genomic target. While 5′-truncated L1 elements show a statistically significant preference for short patches of overlapping nucleotides between their target site and the point of truncation, full-length insertions display no distinct bias for such microhomologies at their 5′-ends. In a second genome-wide approach, we analyzed Alu elements to examine whether these nonautonomous retrotransposons, which are thought to be mobilized through L1 proteins, show similar characteristics. We found that Alu elements appear to be predominantly integrated via a pathway not involving overlapping nucleotides. The results indicate that a cellular nonhomologous DNA end-joining pathway may resolve intermediates from incomplete L1 retrotransposition events and thus lead to 5′ truncations.
    Type of Medium: Online Resource
    ISSN: 1088-9051
    URL: Article
    DOI: 10.1101/gr.3421505
    RVK:
    XA 10000
    Language: English
    Publisher: Cold Spring Harbor Laboratory
    Publication Date: 2005
    detail.hit.zdb_id: 1483456-X
    SSG: 12
    Location Call Number Limitation Availability
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  • 3
    Online Resource
    Online Resource
    Retrotransposons in the development and progression of amyotrophic lateral sclerosis
    BMJ ; 2019
    In:  Journal of Neurology, Neurosurgery & Psychiatry Vol. 90, No. 3 ( 2019-03), p. 284-293
    Details
    In: Journal of Neurology, Neurosurgery & Psychiatry, BMJ, Vol. 90, No. 3 ( 2019-03), p. 284-293
    Abstract: Endogenous retrotransposon sequences constitute approximately 42% of the human genome, and mobilisation of retrotransposons has resulted in rearrangements, duplications, deletions, novel transcripts and the introduction of new regulatory domains throughout the human genome. Both germline and somatic de novo retrotransposition events have been involved in a range of human diseases, and there is emerging evidence for the modulation of retrotransposon activity during the development of specific diseases. Particularly, there is unequivocal consensus that endogenous retrotransposition can occur in neuronal lineages. This review addresses our current knowledge of the different mechanisms through which retrotransposons might influence the development of and predisposition to amyotrophic lateral sclerosis.
    Type of Medium: Online Resource
    ISSN: 0022-3050 , 1468-330X
    URL: Article
    URL: Article
    DOI: 10.1136/jnnp-2018-319210
    DOI: 10.1136/jnnp-2018-319210.supp1
    RVK:
    XA 10000
    Language: English
    Publisher: BMJ
    Publication Date: 2019
    detail.hit.zdb_id: 1480429-3
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  • 4
    Online Resource
    Online Resource
    Trex-1 deficiency in rheumatoid arthritis synovial fibroblasts
    Wiley ; 2010
    In:  Arthritis & Rheumatism Vol. 62, No. 9 ( 2010-09), p. 2673-2679
    Details
    In: Arthritis & Rheumatism, Wiley, Vol. 62, No. 9 ( 2010-09), p. 2673-2679
    Type of Medium: Online Resource
    ISSN: 0004-3591
    URL: Article
    DOI: 10.1002/art.27567
    RVK:
    XA 10000
    RVK:
    XA 30325
    Language: English
    Publisher: Wiley
    Publication Date: 2010
    detail.hit.zdb_id: 2754614-7
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