Evolutionary dynamism of the primate LRRC37 gene family
- Giuliana Giannuzzi1,
- Priscillia Siswara2,
- Maika Malig2,
- Tomas Marques-Bonet3,
- NISC Comparative Sequencing Program4,
- James C. Mullikin4,
- Mario Ventura1,2 and
- Evan E. Eichler2,5,6
- 1Dipartimento di Biologia, Università degli Studi di Bari “Aldo Moro,” Bari 70126, Italy;
- 2Department of Genome Sciences, University of Washington School of Medicine, Seattle, Washington 98195, USA;
- 3IBE, Institut de Biologia Evolutiva (UPF-CSIC), Universitat Pompeu Fabra, PRBB, 08003 Barcelona, Catalonia, Spain;
- 4Genome Technology Branch and NIH Intramural Sequencing Center (NISC), National Human Genome Research Institute, Bethesda, Maryland 20892, USA;
- 5Howard Hughes Medical Institute, University of Washington, Seattle, Washington 98195, USA
Abstract
Core duplicons in the human genome represent ancestral duplication modules shared by the majority of intrachromosomal duplication blocks within a given chromosome. These cores are associated with the emergence of novel gene families in the hominoid lineage, but their genomic organization and gene characterization among other primates are largely unknown. Here, we investigate the genomic organization and expression of the core duplicon on chromosome 17 that led to the expansion of LRRC37 during primate evolution. A comparison of the LRRC37 gene family organization in human, orangutan, macaque, marmoset, and lemur genomes shows the presence of both orthologous and species-specific gene copies in all primate lineages. Expression profiling in mouse, macaque, and human tissues reveals that the ancestral expression of LRRC37 was restricted to the testis. In the hominid lineage, the pattern of LRRC37 became increasingly ubiquitous, with significantly higher levels of expression in the cerebellum and thymus, and showed a remarkable diversity of alternative splice forms. Transfection studies in HeLa cells indicate that the human FLAG-tagged recombinant LRRC37 protein is secreted after cleavage of a transmembrane precursor and its overexpression can induce filipodia formation.
Footnotes
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↵6 Corresponding author
E-mail eee{at}gs.washington.edu
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[Supplemental material is available for this article.]
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Article published online before print. Article, supplemental material, and publication date are at http://www.genome.org/cgi/doi/10.1101/gr.138842.112.
- Received February 13, 2012.
- Accepted October 2, 2012.
This article is distributed exclusively by Cold Spring Harbor Laboratory Press for the first six months after the full-issue publication date (see http://genome.cshlp.org/site/misc/terms.xhtml). After six months, it is available under a Creative Commons License (Attribution-NonCommercial 3.0 Unported License), as described at http://creativecommons.org/licenses/by-nc/3.0/.
