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However, the direct links between the deleterious mutations or deletions in these two genes and several human disorders, such as inherited inflammatory calcified tumors and acute myeloid leukemia, suggest their biological importance. SAMD9 and SAMD9L have also recently been shown to play key roles in the innate immune responses to stimuli such as viral infection. We were particularly interested in understanding the mammalian evolutionary history of these two genes. The phylogeny of<jats:italic>SAMD9<\/jats:italic>and<jats:italic>SAMD9L<\/jats:italic>genes was reconstructed using the Maximum Likelihood method. Furthermore, six different methods were applied to detect SAMD9 and SAMD9L codons under selective pressure: the site-specific model M8 implemented in the codeml program in PAML software and five methods available on the Datamonkey web server, including the Single Likelihood Ancestor Counting method, the Fixed Effect Likelihood method, the Random Effect Likelihood method, the Mixed Effects Model of Evolution method and the Fast Unbiased Bayesian AppRoximation method. Additionally, the house mouse (<jats:italic>Mus musculus<\/jats:italic>) genome has lost the<jats:italic>SAMD9<\/jats:italic>gene<jats:italic>,<\/jats:italic>while keeping<jats:italic>SAMD9L<\/jats:italic>intact, prompting us to investigate whether this loss is a unique event during evolution.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>Our evolutionary analyses suggest that<jats:italic>SAMD9<\/jats:italic>and<jats:italic>SAMD9L<\/jats:italic>arose through an ancestral gene duplication event after the divergence of Marsupialia from Placentalia. Additionally, selection analyses demonstrated that both genes have been subjected to positive evolutionary selection. The absence of either<jats:italic>SAMD9<\/jats:italic>or<jats:italic>SAMD9L<\/jats:italic>genes from some mammalian species supports a partial functional redundancy between the two genes.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p>To the best of our knowledge, this work is the first study on the evolutionary history of mammalian<jats:italic>SAMD9<\/jats:italic>and<jats:italic>SAMD9L<\/jats:italic>genes. We conclude that evolutionary selective pressure has acted on both of these two genes since their divergence, suggesting their importance in multiple cellular processes, such as the immune responses to viral pathogens.<\/jats:p><\/jats:sec>","DOI":"10.1186\/1471-2148-13-121","type":"journal-article","created":{"date-parts":[[2013,6,12]],"date-time":"2013-06-12T08:14:17Z","timestamp":1371024857000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":56,"title":["Evolution and divergence of the mammalian SAMD9\/SAMD9L gene family"],"prefix":"10.1186","volume":"13","author":[{"given":"Ana","family":"Lemos de Matos","sequence":"first","affiliation":[]},{"given":"Jia","family":"Liu","sequence":"additional","affiliation":[]},{"given":"Grant","family":"McFadden","sequence":"additional","affiliation":[]},{"given":"Pedro J","family":"Esteves","sequence":"additional","affiliation":[]}],"member":"297","published-online":{"date-parts":[[2013,6,12]]},"reference":[{"key":"2355_CR1","doi-asserted-by":"publisher","first-page":"92","DOI":"10.1186\/1471-2164-8-92","volume":"8","author":"CF Li","year":"2007","unstructured":"Li CF, MacDonald JR, Wei RY, Ray J, Lau K, Kandel C, Koffman R, Bell S, Scherer SW, Alman BA: Human sterile alpha motif domain 9, a novel gene identified as down-regulated in aggressive fibromatosis, is absent in the mouse. 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