| Summary: | <p>Abstract</p> <p>Background</p> <p>In <it>Xenopus </it>retinogenesis, p27Xic1, a <it>Xenopus </it>cyclin dependent kinase inhibitor, functions as a cell fate determinant in both gliogenesis and neurogenesis in a context dependent manner. This activity is essential for co-ordination of determination and cell cycle regulation. However, very little is known about the mechanism regulating the context dependent choice between gliogenesis versus neurogenesis.</p> <p>Results</p> <p>We have identified NM23-X4, a NM23 family member, as a binding partner of p27Xic1. NM23-X4 is expressed at the periphery of the ciliary marginal zone of the <it>Xenopus </it>retina and the expression overlaps with p27Xic1 at the central side. Our <it>in vivo </it>functional analysis in <it>Xenopus </it>retina has shown that knockdown of NM23-X4 activates gliogenesis. Furthermore, co-overexpression of NM23-X4 with p27Xic1 results in the inhibition of p27Xic1-mediated gliogenesis, through direct interaction of NM23-X4 with the amino-terminal side of p27Xic1. This inhibitory effect on gliogenesis requires serine-150 and histidine-148, which correspond to the important residues for the kinase activities of NM23 family members.</p> <p>Conclusion</p> <p>This study demonstrates that NM23-X4 functions as an inhibitor of p27Xic1-mediated gliogenesis in <it>Xenopus </it>retina and suggests that this activity contributes to the proper spatio-temporal regulation of gliogenesis.</p>
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