Aquaporins (AQPs ) are a family of transmembrane proteins present in almost all species including virus. They are grossly divided into three subfamilies based on the sequence around a highly conserved pore-forming NPA motif: (1) classical water -selective AQP (CAQP), (2) glycerol -permeable aquaglyceroporin (AQGP) and (3) AQP super-gene channel, superaquaporin (SAQP). AQP is composed of two tandem repeats of conserved three transmembrane domains and a NPA motif. AQP ancestors probably started in prokaryotes by the duplication of half AQP genes to be diversified into CAQPs or AQGPs by evolving a subfamily-specific carboxyl-terminal NPA motif. Both AQP subfamilies may have been carried over to unicellular eukaryotic ancestors, protists and further to multicellular organisms. Although fungus lineage has kept both AQP subfamilies, the plant lineage has lost AQGP after algal ancestors with extensive diversifications of CAQPs into PIP, TIP, SIP, XIP, HIP and LIP with a possible horizontal transfer of NIP from bacteria. Interestingly, the animal lineage has obtained new SAQP subfamily with highly deviated NPA motifs, especially at the amino-terminal halves in both prostomial and deuterostomial animals. The prostomial lineage has lost AQGP after hymenoptera, while the deuterostomial lineage has kept all three subfamilies up to the vertebrate with diversified CAQPs (AQP0, 1, 2, 4, 5, 6, 8) and AQGPs (AQP3, 7, 9, 10) with limited SAQPs (AQP11, 12) in mammals. Whole-genome duplications, local gene duplications and horizontal gene transfers may have produced the AQP diversity with adaptive selections and functional alternations in response to environment changes. With the above evolutionary perspective in mind, the function of each AQP could be speculated by comparison among species to get new insights into physiological roles of AQPs . This evolutionary guidance in AQP research will lead to deeper understandings of water and solute homeostasis.

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Neural crest is formed at the boundary of epidermal and neural ectoderm. To understand the molecular mechanism of neural crest formation, we focused on the transcriptional regulation of the Slug gene. In the upstream sequence of the chicken Slug gene, we have identified potential binding sites for transcription factors, such as Lef / Tcf and Smad1. Transgenic mouse embryos carrying the chicken Slug promoter-reporter gene showed a crest-specific activation of the reporter, suggesting the isolated sequence included the cis-regulatory elements to receive Slug-inducing signals in the mouse neural crest. While these potential cis-regulatory elements could be recognized and activated by corresponding transcription factors, such as Lef1 and Smad1, Wnt-Lef-β-catenin signal failed to induce endogenous Slug expression in quail neural plate tissue prepared from forebrain and midbrain levels. In contrast, Slug expression and subsequent epithelialmesenchymal transition were effectively induced by BMP4. Consistently, while we could detect phosphorylation of Smad1 in the ectoderm including the neural plate and the neural fold region, the activation of a reporter gene for a detection of canonical Wnt signal activation was below the level of detection at the forebrain and midbrain levels. These observations indicated that in the anterior ectoderm BMP signal has a predominant role for Slug expression.

Early neural patterning along the anteroposterior (AP) axis appears to involve a number of signal transducing pathways, but the precise role of each of these pathways for AP patterning and how they are integrated with signals that govern neural induction step is not well understood. We investigate the nature of Fgf response element (FRE) in a posterior neural gene, Xcad3 (Xenopus caudal homologue) that plays a crucial role of posterior neural development. We provide evidence that FREs of Xcad3 are widely dispersed in its intronic sequence and that these multiple FREs comprise Ets-binding and Tcf/Lef-binding motifs that lie in juxtaposition. Functional and physical analyses indicate that signaling pathways of Fgf, Bmp and Wnt are integrated on these FREs to regulate the expression of Xcad3 in the posterior neural tube through positively acting Ets and Sox family transcription factors and negatively acting Tcf family transcription factor(s).