RU T H B . M c C O L E E T A L . Figure 5. Expression for mouse retrogenes and their parent genes during spermatogenesis. GC RMA values for two biological replicates were averaged. Data were extracted from GEO dataset GDS2930 from Namekawa et al 2006. Probe identiﬁers were 1425018_at for Mcts1, 1451058_at for Mcts2, 1417411_at for Nap1l5, 1418046_at for Nap1l2, 1449354_at for U2af1-rs1, and 1455727_at for U2af1-rs2. There was no speciﬁc probe for Inpp5f_v2, so this gene could not be included. not to have a testis-specific expression pattern, but to be expressed in 14 of 14 somatic tissues examined. This finding complements the results presented here nicely. Retrogenes are also said to emerge “out of the testes” (Vinck- enbosch et al. 2006), as this tissue exhibits very high levels of tran- scription. Retrogenes might then go on to evolve a more broad expression pattern. Surprisingly, although the four imprinted ret- rogenes discussed here are of quite different ages, with U2af1-rs1 the youngest, and Mcts2 and Nap1l5 older, all retrogenes display a very broad expression pattern, which in each case is similar to their parent gene. Hence, the retrogenes studied here do not seem to have emerged “out of the testis.” This is perhaps not surprising, as these retrogenes already differ from most by their imprinted status, and their position within the introns of other “host” genes. Perhaps the presence of the host gene confers a wide expression pattern on the retrogenes via access to a transcriptionally active genomic environment (L. Potrzebowski, pers. comm.). Mcts2 AS A POTENTIAL ONCOGENE In humans, the Mcts1 (Mct-1) gene has been established as having oncogenic properties (Hsu et al. 2005, 2007). Like the U2af1-rs proteins, Mcts1 is an RNA-binding protein. Mcts1 binds RNA via a PUA domain and appears to alter cellular phenotype by inter- acting with mRNA and affecting translation (Reinert et al. 2006; Mazan-Mamczarz et al. 2009). Given the similarity of all the Mcts family genes, as shown by the MSA, and the high level of puri- fying selection present across all residues of these genes across multiple species, it seems likely that Mcts2 and its orthologs may share similar functions and may also have oncogenic properties. There is a strong link between the phenomenon of imprinting and cancer etiology (Feinberg 2007). Considering that Mcts2 is sub- ject to genomic imprinting, as is Mcts2, potential disruption of the imprinting mechanism at the Mcts2 locus could have major consequences for cancer development if Mcts2 is shown to be an oncogene. 1 4 2 4 EVOLUTION MAY 2011