Abstract
Members of the disintegrin metalloproteinase (ADAM) family have important functions in regulating cell-cell and cell-matrix interactions as well as cell signaling. There are two major types of ADAMs: the somatic ADAMs (sADAMs) that have a significant presence in somatic tissues, and the testicular ADAMs (tADAMs) that are expressed predominantly in the testis. Genes encoding tADAMs can be further divided into two groups: group I (intronless) and group II (intron-containing). To date, tAdams have only been reported in placental mammals, and their evolutionary origin and relationship to sAdams remain largely unknown. Using phylogenetic and syntenic tools, we analyzed the Adam genes in various vertebrates ranging from fishes to placental mammals. Our analyses reveal duplication and loss of some sAdams in certain vertebrate species. In particular, there exists an Adam9-like gene in non-mammalian vertebrates but not mammals. We also identified putative group I and group II tAdams in all amniote species that have been examined. These tAdam homologues are more closely related to Adams 9 and 9-like than to other sAdams. In all amniote species examined, group II tAdams lie in close vicinity to Adam9 and hence likely arose from tandem duplication, whereas group I tAdams likely originated through retroposition because of their lack of introns. Clusters of multiple group I tAdams are also common, suggesting tandem duplication after retroposition. Therefore, Adam9/9-like and some of the derived tAdam loci are likely preferred targets for tandem duplication and/or retroposition. Consistent with this hypothesis, we identified a young retroposed gene that duplicated recently from Adam9 in the opossum. As a result of gene duplication, some tAdams were pseudogenized in certain species, whereas others acquired new expression patterns and functions. The rapid duplication of Adam genes has a major contribution to the diversity of ADAMs in various vertebrate species.
Highlights
The first two members of the ADAM family were originally identified as guinea pig sperm-surface antigens that were recognized by the monoclonal antibody PH-30, which strongly inhibits sperm-egg fusion [1]
Phylogenetic and syntenic analyses suggest that these tAdams originally derived from ancient Adam9, a somatic Adam that is conserved in vertebrates, and/or Adam9-like, which we identified here as a close paralogue of Adam9
In this study we show that certain Adam genes were frequently lost or duplicated during vertebrate evolution
Summary
The first two members of the ADAM family were originally identified as guinea pig sperm-surface antigens that were recognized by the monoclonal antibody PH-30, which strongly inhibits sperm-egg fusion [1]. Sequence analyses of the precursors of both proteins showed that they have a domain organization similar to that of snake venom metalloproteinases, containing a disintegrin domain and a metalloproteinase domain [2,3]. Genes encoding these two proteins, together with several homologues that were cloned from guinea pig and mouse testis, were renamed “Adams” (a disintegrin and metalloproteinases) to reflect these important features [4]. ADAMs have been implicated in many diseases, including tumors, immune diseases and neurodegenerative diseases [7,8]
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