Re: Junk DNA again

From: Rich Blinne (e-lists@blinne.org)
Date: Fri May 23 2003 - 20:18:04 EDT

  • Next message: Don Winterstein: "Re: On Tillich"

    On Fri, 23 May 2003 15:33:23 -0400, "bivalve"
    <bivalve@mail.davidson.alumlink.com> said:
    > The latest Science has another example of purportedly junk DNA having
    > usefulness; unfortunately for the current ID movement, it is evolutionary
    > usefulness. Here's their summary:
    >
    > This Week in SCIENCE, Volume 300, Issue 5623,
    > dated May 23 2003
    > Putting DNA Sequences Back to Work
    >
    > Repetitive Alu sequences are part of the nonprotein coding "junk" DNA,
    > but mutations in these sequences can form coding exons. Although this
    > process is associated with disease in some cases, it also is a way for
    > the genome to evolve. Lev-Maor et al. (p. 1288; see the Perspective by
    > Makalowski)
    > have assembled a database of "exonized" Alu elements and identified the
    > particular sequences and positions that can allow the crucial splicing to
    > occur. They tested their proposed mechanism in a mini-gene construct and
    > found that a single mutation can result in exonization.
    >

    In the 1 May 2003 Nature there was another article on the function of
    non-coding genes:

    An expressed pseudogene regulates the messenger-RNA stability of its
    homologous coding gene

    SHINJI HIROTSUNE*†, NORIYUKI YOSHIDA*, AMY CHEN‡, LISA GARRETT‡, FUMIHIRO
    SUGIYAMA§, SATORU TAKAHASHI§, KEN-ICHI YAGAMI§, ANTHONY WYNSHAW-BORIS‡ &
    ATSUSHI YOSHIKI¶

    * Division of Neuroscience, Research Center for Genomic Medicine, Saitama
    Medical School Yamane 1397-1, Hidaka City, Saitama 350-1241, Japan
    † PRESTO, Japan Science and Technology Corporation, Hon-cho 4-1-8,
    Kawaguchi, Saitama, Japan
    ‡ Genetic Disease Research Branch, National Human Genome Research
    Institute, NIH, Bldg 49, Room 4C80 49, Convent Drive, Bethesda, Maryland
    20892, USA
    § Institute of Basic Medical Sciences and Laboratory Animal Resource
    Center, University of Tsukuba, 1-1-1 Tennodai, Tsukuba, Ibaraki 305-8575,
    Japan
     Departments of Pediatrics and Medicine, UCSD Cancer Center, University
     of California, San Diego School of Medicine, 9500 Gilman Drive, Mailstop
     0627, La Jolla, California 92093-0627, USA
    ¶ Experimental Animal Division, Department of Biological Systems,
    BioResource Center, RIKEN Tsukuba Institute, 3-1-1 Koyadai, Tsukuba,
    Ibaraki 305-0074, Japan

    Correspondence and requests for materials should be addressed to S.H.
    (shinjih@saitama-med.ac.jp).

    A pseudogene is a gene copy that does not produce a functional,
    full-length protein. The human genome is estimated to contain up to
    20,000 pseudogenes. Although much effort has been devoted to
    understanding the function of pseudogenes, their biological roles remain
    largely unknown. Here we report the role of an expressed
    pseudogene—regulation of messenger-RNA stability—in a transgene-insertion
    mouse mutant exhibiting polycystic kidneys and bone deformity. The
    transgene was integrated into the vicinity of the expressing pseudogene
    of Makorin1, called Makorin1-p1. This insertion reduced transcription of
    Makorin1-p1, resulting in destabilization of Makorin1 mRNA in trans by
    way of a cis-acting RNA decay element within the 5' region of Makorin1
    that is homologous between Makorin1 and Makorin1-p1. Either Makorin1 or
    Makorin1-p1 transgenes could rescue these phenotypes. Our findings
    demonstrate a specific regulatory role of an expressed pseudogene, and
    point to the functional significance of non-coding RNAs.



    This archive was generated by hypermail 2.1.4 : Fri May 23 2003 - 20:18:36 EDT