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Research from the Batzer laboratory featured on the cover of PNAS again



A paper from Dr. Batzerīs laboratory reporting retrotransposon-mediated gene transduction is featured on the cover of the November 21st, 2006 issue of PNAS. The paper describes the evolutionary history that led to the formation of the AMAC gene family after SVA retrotransposon-mediated gene transduction in the primate lineage.  The work provides direct evidence for the impact of mobile elements on their host genomes and a molecular mechanism for the creation of new gene families.

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Cover Legend: The 24 human chromosomes showing all of the SVA mobile element-mediated sequence transduction events mapped to individual chromosomes (shown as light lines and dots). SVA is a composite retrotransposon named for its main components: SINE, VNTR, and Alu. Gene duplication and transduction events for the acyl-malonyl condensing enzyme (AMAC) gene are shown as red lines; AMAC is an enzyme involved in fatty acid synthesis. See the article by Xing et al. on pages 17608–17613. Image courtesy of Bang Wong (ClearScience, Cambridge, MA), Jinchuan Xing, and Mark A. Batzer; the single copies of each chromosome are adapted from a human male karyotype image (Copyright 2003, Howard Hughes Medical Institute).

Abstract

Gene duplication is one of the most important mechanisms for creating new genes and generating genomic novelty. Retrotransposon-mediated sequence transduction (i.e., the process by which a retrotransposon carries flanking sequence during its mobilization) has been proposed as a gene duplication mechanism. L1 exon shuffling potential has been reported in cell culture assays, and two potential L1-mediated exon shuffling events have been identified in the genome. SVA is the youngest retrotransposon family in primates and is capable of 3' flanking sequence transduction during retrotransposition. In this study, we examined all of the full-length SVA elements in the human genome to assess the frequency and impact of SVA-mediated 3' sequence transduction. Our results showed that {approx} 53 kb of genomic sequences have been duplicated by 143 different SVA-mediated transduction events. In particular, we identified one group of SVA elements that duplicated the entire AMAC gene three times in the human genome through SVA-mediated transduction events, which happened before the divergence of humans and African great apes. In addition to the original AMAC gene, the three transduced AMAC copies contain intact ORFs in the human genome, and at least two are actively transcribed in different human tissues. The duplication of entire genes and the creation of previously undescribed gene families through retrotransposon-mediated sequence transduction represent an important mechanism by which mobile elements impact their host genomes.

Ref: Xing, J.*, H. Wang*, V. P. Belancio, R. Cordaux, P. L. Deininger and M. A. Batzer (2006) Emergence of primate genes by retrotransposon-mediated sequence transduction. Proceedings of the National Academy of Sciences, USA 103: 17608-17613.  ( pdf )

* These authors contributed equally to this work.

Other links: PNAS special feature on Eukaryotic Transposable Elements and Genome Evolution       List of papers

 

Additional information about research projects in the Batzer lab is available from the laboratory web site http://batzerlab.lsu.edu