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¹ Division of Integrative Cell Biology, Institute of Molecular Embryology and Genetics, Kumamoto University, Kumamoto 860-0811, Japan
² Division of Biological Functional Science, Graduate School of Life and Environmental Science, University of Tsukuba, Ibaraki 305-8572, Japan
³ Division of Stem Cell Regulation, The Institute of Medical Science, The University of Tokyo, Tokyo 108-8639, Japan
⁴ Department of Life Sciences, The University of Tokyo, Tokyo 153-8902, Japan

The Spalt (sal) gene family is conserved from Drosophila to humans. Mutations of human SALL1 cause Townes–Brocks syndrome, with features of ear, limb, anal, renal and heart anomalies. Sall1, a murine homolog of SALL1, is essential for kidney formation, and both Sall1 and SALL1 localize to heterochromatin in the nucleus. Here, we present a molecular mechanism for the heterochromatin localization of Sall1. Mutation analyses revealed that the 7th–10th C-terminal double zinc finger motifs were required for the localization. A recombinant protein of the most C-terminal double zinc finger (9th–10th) bound to specific A/T-rich sequences. Furthermore, Sall1 associated with A/T-rich sequences of the major satellite DNA in heterochromatin. Thus Sall1 may bind to A/T-rich sequences of the major satellite DNA via its C-terminal double zinc fingers, thereby mediating its localization to heterochromatin.

^aThese two authors contributed equally to this work.

^* Correspondence: E-mail: ryuichi{at}kaiju.medic.kumamoto-u.ac.jp

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