in the liver and the relative levels of SRp40, hnRNP A2/B2 and Srp54 messages were consistently lower. A well established paradigm in the field of RNA splicing is that usage of alternative splice sites is often controlled by the relative concentrations of specific SR proteins and hnRNP proteins [49-52]. This functional antagonism between particular SR and hnRNP proteins is often due to competition for binding of nearby sites on pre-mRNAs [49,53,54]. Therefore, it seems likely that the unusual patterns of expression seen in the human adult liver for these families of splicing factors may contribute to the high level of alternative splice site usage seen in this tissue. It is also interesting that splicing-factor expression in the human fetal liver is highly concordant with most other tissues, but has low concordance with the adult liver (Figure 3). This observation suggests that substantial changes in splicing-factor expression may occur during human liver development, presumably leading to a host of changes in the splicing patterns of genes expressed in human liver. Currently available EST data were insufficient to allow systematic analysis of the patterns of AS in fetal relative to adult liver.
