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J. Biol. Chem., Vol. 278, Issue 50, 50386-50392, December 12, 2003

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Identification of a Novel Glial Cell Line-derived Neurotrophic Factor-inducible Gene Required for Renal Branching Morphogenesis^*

Naoyuki Fukuda, Masatoshi Ichihara, Takatoshi Morinaga, Kumi Kawai¶, Hironori Hayashi, Yoshiki Murakumo, Seiichi Matsuo, and Masahide Takahashi¶||

From the Departments of Pathology and Internal Medicine, Nagoya University Graduate School of Medicine, 65 Tsurumai-cho, Showa-ku, Nagoya 466-8550, Japan and the ^¶Division of Molecular Pathology, Center for Neural Disease and Cancer, Nagoya University Graduate School of Medicine, 65 Tsurumai-cho, Showa-ku, Nagoya 466-8550, Japan

In the developing kidney, activation of the rearrangement during transfection by glial cell line-derived neurotrophic factor (GDNF) is required for normal branching of the ureteric bud epithelium. By differential display analysis we identified a novel GDNF-inducible gene (named GZF1) with a BTB/POZ (broad complex, tramtrack, and bric-a-brac)/(poxvirus and zinc finger) domain and 10 tandemly repeated zinc finger motifs. The up-regulation of the GZF1 gene showed two peaks at 1 h and 24–48 h after GDNF stimulation by Northern blotting. The late induction was also found at protein levels by Western blotting with anti-GZF1 antibody. As observed for other proteins with the BTB/POZ domain, the GZF1 protein had strong transcriptional repressive activity. Intriguingly, its expression was detected at high levels in branching ureteric buds and collecting ducts of mouse metanephric kidney in which RET was also expressed. Antisense phosphorothioated oligodeoxynucleotides of the GZF1 gene markedly impaired the ureteric bud branching in the metanephric organ culture, suggesting that the induction of GZF1 expression via the GDNF/RET signaling system is required for renal branching morphogenesis.

Received for publication, August 29, 2003

The nucleotide sequence(s) reported in this paper has been submitted to the DDBJ/GenBank^TM/EBI Data Bank with accession number(s) AB100265 and AB100266.

^* This work was supported by grants-in-aid for Center of Excellence research and scientific research from the Ministry of Education, Culture, Sports, Science, and Technology of Japan. The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

^|| To whom correspondence should be addressed. Fax: 81-52-744-2098; E-mail: mtakaha{at}med.nagoya-u.ac.jp.

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