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Mammalian Genome

, Volume 10, Issue 7, pp 662–669 | Cite as

Genomic organization and expression analysis of the mouse qkI locus

  • Tatsuya  Kondo
  • Tokiko  Furuta
  • Kanae  Mitsunaga
  • Thomas A.  Ebersole
  • Motoaki  Shichiri
  • Jiang  Wu
  • Karen  Artzt
  • Ken-ichi  Yamamura
  • Kuniya  Abe

Abstract.

qkI, encoding a KH domain-containing RNA binding protein, has been isolated as a candidate gene for the mouse neurological mutation quaking. Here, we describe detailed studies on its genomic structure and expression pattern. We isolated approximately 1 Mb of genomic region containing the quaking locus and determined its genomic organization. The qkI locus contains at least 9 exons spanning ∼65 kb of DNA. It gives rise to six distinct transcripts encoding, theoretically, five different protein isoforms. Exons 1 through 4 are shared by all the transcripts, whereas coding exons and two distinct 3′-UTRs downstream to the exon 4 are differentially utilized. One isoform has a truncated KH domain and may act as an antagonist to the others. These findings and identification of a single transcription initiation site suggest that differential expression of each transcript is regulated by alternative splicing. Expression of each alternative transcript and protein product was also examined. Two types of transcripts, 5 kb-A and B, are most abundant in the brain of newborn mice and are gradually downregulated thereafter. In contrast, the other three messages, 6 kb, 7 kb-A and B, increase as myelination proceeds and peak at 2 weeks of age, corresponding to the most active stage of myelination. Although the qkI messages and their products are abundant in brain and heart, a lower level of expression was found in various other tissues tested. Alternative transcripts that share the same 3′-UTR showed very similar expression patterns, suggesting a regulatory role of the 3′-UTRs in qkI gene expression.

Keywords

Genomic Region Alternative Splice Initiation Site Genomic Organization Genomic Structure 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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Copyright information

© Springer-Verlag New York Inc. 1999

Authors and Affiliations

  • Tatsuya  Kondo
    • 1
  • Tokiko  Furuta
    • 1
  • Kanae  Mitsunaga
    • 1
  • Thomas A.  Ebersole
    • 2
  • Motoaki  Shichiri
    • 3
  • Jiang  Wu
    • 4
  • Karen  Artzt
    • 4
  • Ken-ichi  Yamamura
    • 1
  • Kuniya  Abe
    • 1
  1. 1.Institute of Molecular Embryology and Genetics, Kumamoto University School of Medicine, 4-24-1 Kuhonji, Kumamoto 862-0976, JapanJP
  2. 2.Human Genetics Unit, Western General Hospital, Edinburgh EH4 2XU, UKGB
  3. 3.Department of Metabolic Medicine, Kumamoto University School of Medicine, 1-1-1 Honjo, Kumamoto 860-0811, JapanJP
  4. 4.Institute for Cell and Molecular Biology and Department of Microbiology, The University of Texas at Austin, Austin, Texas, 78712-1064, USAUS

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