Specific Fatal 3-deazaneplanocin A Errors You May End Up Doing

, 2003). Multiple publications Selleckchem 3-deazaneplanocin A have suggested that this gene plays an important role in maintaining pluripotency and inhibiting differentiation into the three primary tissue germ layers (Masui et al., 2008; Scotland et al., 2009; Son et al., 2013), with multiple mechanisms of action having been proposed. However, REX1-knockout mouse ESC lines can give rise to chimeric animals, and homozygous F2 REX1 null mice are viable (Masui et al., 2008), suggesting that REX1 may not be indispensable for murine pluripotency. In humans, loss of REX1 expression in ESCs following shRNA knockdown has been associated with a rapid loss of pluripotency, as well as a decrease in glycolytic activity and a lack of observable mature mesodermal structures in teratoma formation assays (Son et al., 2013). To determine the consequences of a lack of REX1 expression in chimpanzee iPSCs, we considered gene expression data from all human iPSC lines and the 6 chimpanzee iPSC lines that do not express REX1. We asked whether there is an excess of DE Ro3280 genes among those thought to be directly regulated by, or downstream of, REX1 (Figure 6C,D; see ��Materials and methods��), but failed to find enrichment in all categories except for genes associated with GO term BP:0006096, glycolysis, where 19 of 34 testable genes were DE at an FDR of 1% between the two species (p Erastin ic50 such as PGAM1 or LDHA, having significantly higher expression in chimpanzee iPSCs than in human iPSCS (Figure 6D). Furthermore, the REX1-expressing line C6 is not an outlier amongst the other chimpanzee iPSC lines (Figure 6D), suggesting that the observed inter-species regulatory differences cannot be attributed to differences in REX1 expression between the species. We note that both the teratomas and EBs generated from chimpanzee iPSC lines that do not express REX1 gave rise to mature structures from all three germ layers similar to those observed in REX1-expressing line C6 (Figure 2��figure supplements 1, 3). Furthermore, and consistent with our observations, REX1 is either absent or expressed at low levels in one replicate of either of the two retrovirally reprogrammed bonobo (Pan paniscus, sister species to chimpanzees) iPSC lines generated by Marchetto et al. (2013b), although it is expressed in both replicates of both chimpanzee iPCS lines from the same group (Figure 6��figure supplement 2). Together, these findings suggest that that the variable loss of REX1 expression in chimpanzee and bonobo iPSCs does not impair pluripotency, and that its regulatory functions of in humans may be being fulfilled in chimpanzee iPSCs by other regulatory mechanisms.