International Mammalian Genome Society

17th International Mouse Genome Conference

9-12 November 2003, Braunschweig, Germany


POSTER 66 - SPROUTY4 (SPRY4) IS ESSENTIAL FOR CORRECT LIMB FORMATION

Vauti F
Department of Cell- & Molecular Biology, Institute of Biochemistry and Biotechnology, Technical University of Braunschweig, Spielmannstrasse 7, D-38106 Braunschweig

Co-Authors: Suresh Kumar R, Arnold HH
Institutions: Department of Cell- & Molecular Biology, Institute of Biochemistry and Biotechnology, Technical University of Braunschweig, Spielmannstrasse 7, D-38106 Braunschweig

Sprouty is believed to negatively modulate FGF signaling. To investigate the role of Spry4 during mouse development, we used a gene trap integration disrupting the Spry4 gene. At E8.5 the gene trap reporter is expressed in the forebrain and tail bud. Between E9.5 and E10.5 Spry4 expression commences in the mid-hind brain boundary, nasal placodes, branchial arches, somites and limb buds. In the adult mouse Spry4 expression was found in brain, lung, liver and testis. Homozygous Spry4 mutants display malformations of forelimbs with various defects in autopods but not in stylopods or zeugopods. Dysmorphogenesis of the hand plate varies among individual mutant animals and shows syndactyly, missing digits as well as extra digits on the ventral side. At E11.5 the AER appears locally disrupted lacking FGF8 and FGF4 expression. In these regions massive loss of underlying mesenchyme is observed. Shh expression emanating from the ZPA is not altered in mutants consistent with normal AP patterning of the limb buds. These observations suggest that Spry4 is necessary to maintain the AER and to prevent premature apoptosis of the interdigital web.


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