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Böhm, J.* ; Buck, A.* ; Borozdin, W.* ; Mannan, A.U.* ; Matysiak-Scholze, U.* ; Adham, I.* ; Schulz-Schaeffer, W.* ; Floß, T. ; Wurst, W. ; Kohlhase, J.* ; Barrionuevo, F.*

Sall1, Sall2, and Sall4 Are Required for Neural Tube Closure in Mice.

Am. J. Pathol. 173, 1455-1463 (2008)

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Open Access Green möglich sobald Postprint bei der ZB eingereicht worden ist.

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Four homologs to the Drosophila homeotic gene spalt (sat) exist in both humans and mice (SALL1 to SALL4/Sall1 to Sall4, respectively). Mutations in both SALL1 and SALL4 result in the autosomal-dominant developmental disorders Townes-Brocks and Okihiro, syndrome, respectively. in contrast, no human diseases have been associated with SALL2 to date, and Sall2-deficient mice have shown no apparent abnormal phenotype. We generated mice deficient in Sall2 and, contrary to previous reports, 11% of our Sall2-deficient mice showed background-specific neural tube defects, suggesting that Sall2 has a role in neurogenesis. To investigate whether Sall4 may compensate for the absence of Sall2, we generated compound Sall2 knockout/Sall4 genetrap mutant mice. In these mutants, the incidence of neural tube defects was significantly increased. Furthermore, we found a similar phenotype in compound Sall1/4 mutant mice, and in vitro studies showed that SALL1, SALL2, and SALL4 all co-localized in the nucleus. We therefore suggest a fundamental and redundant function of the Sall proteins in murine neurulation, with the heterozygous loss of a particular SALL protein also possibly compensated in humans during development.

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