| First Author | Yamashita K | Year | 2007 |
| Journal | Genes Cells | Volume | 12 |
| Issue | 2 | Pages | 171-82 |
| PubMed ID | 17295837 | Mgi Jnum | J:123390 |
| Mgi Id | MGI:3718183 | Doi | 10.1111/j.1365-2443.2007.01042.x |
| Citation | Yamashita K, et al. (2007) Mouse homolog of SALL1, a causative gene for Townes-Brocks syndrome, binds to A/T-rich sequences in pericentric heterochromatin via its C-terminal zinc finger domains. Genes Cells 12(2):171-82 |
| abstractText | 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. |
