Proceedings of the Japan Academy, Series B

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Studies of the origin of magmas in subduction zones, particularly in the Japanese island arc, have been significantly advanced by petrological, geochemical, geophysical and experimental studies during last 50 years. Kuno's original model¹⁾ for magma generation in the Japanese island arc, that tholeiite magmas are formed at relatively shallow levels in the mantle on the Pacific Ocean side whereas alkali basalt magmas are formed in deeper levels on the Japan Sea side, stimulated subsequent studies, particularly high-pressure experimental studies in which the author participated. Recent seismic tomographic studies of regions beneath the Japanese island arc demonstrate that seismic low-velocity zones where primary magmas are formed have finger-like shapes and rise obliquely from the Japan Sea side toward the Pacific Ocean side. Based on experimental studies, it is suggested that the compositions of primary magmas depend mainly on the H₂O content and degree of melting in the melting zones, and that primary tholeiite magmas are formed by 10-25% melting of the source mantle containing less than 0.2wt.% H₂O. High-alumina basalt and alkali basalt magmas are formed by smaller degrees of melting of similar mantle, whereas primary boninite magmas are formed by more than 20% melting of the source mantle with more than 0.2wt.% H₂O, and finally, high-magnesia andesite magmas are formed by smaller degrees of melting of similar mantle.

(Contributed by Ikuo KUSHIRO, M.J.A.)

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Nemo-like kinase (NLK) is an evolutionarily conserved serine/threonine kinase and has been considered to be a suppressor of Wnt signaling in mammalian cells. Our study, however, has raised the possibility that NLK also functions as a Wnt signaling activator. In human osteosarcoma and neuroblastoma cell lines, NLK specifically enhanced β-catenin-TCF complex transcription activity. The effect required kinase activity of NLK and co-expression of the β-catenin ΔN (constitutive active mutant of β-catenin). The nuclear localization of Lymphoid enhancer factor 1 (LEF1) and β-catenin ΔN was not altered by NLK overexpression regardless of its effect on β-catenin-TCF complex activity. Reporter analysis using LEF1 mutants at known NLK target sites indicated that NLK may have different activation targets for β-catenin-TCF complex. Mutations in the potential NLK phosphorylation sites in β-catenin did not change its transcription activity either. Our results suggest that NLK positively regulates Wnt/β-catenin signaling in a cell type dependent manner through an unidentified mechanism.

(Communicated by Takao SEKIYA, M.J.A.)

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