کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
10933891 1093870 2005 9 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Characteristic defects in neural crest cell-specific Gαq/Gα11- and Gα12/Gα13-deficient mice
موضوعات مرتبط
علوم زیستی و بیوفناوری بیوشیمی، ژنتیک و زیست شناسی مولکولی بیولوژی سلول
پیش نمایش صفحه اول مقاله
Characteristic defects in neural crest cell-specific Gαq/Gα11- and Gα12/Gα13-deficient mice
چکیده انگلیسی
The endothelin/endothelin receptor system plays a critical role in the differentiation and terminal migration of particular neural crest cell subpopulations. Targeted deletion of the G-protein-coupled endothelin receptors ETA and ETB was shown to result in characteristic developmental defects of derivatives of cephalic and cardiac neural crest and of neural crest-derived melanocytes and enteric neurons, respectively. Since both endothelin receptors are coupled to G-proteins of the Gq/G11- and G12/G13-families, we generated mouse lines lacking Gαq/Gα11 or Gα12/Gα13 in neural crest cells to study their roles in neural crest development. Mice lacking Gαq/Gα11 in a neural crest cell-specific manner had craniofacial defects similar to those observed in mice lacking the ETA receptor or endothelin-1 (ET-1). However, in contrast to ET-1/ETA mutant animals, cardiac outflow tract morphology was intact. Surprisingly, neither Gαq/Gα11- nor Gα12/Gα13-deficient mice showed developmental defects seen in animals lacking either the ETB receptor or its ligand endothelin-3 (ET-3). Interestingly, Gα12/Gα13 deficiency in neural crest cell-derived cardiac cells resulted in characteristic cardiac malformations. Our data show that Gq/G11- but not G12/G13-mediated signaling processes mediate ET-1/ETA-dependent development of the cephalic neural crest. In contrast, ET-3/ETB-mediated development of neural crest-derived melanocytes and enteric neurons appears to involve G-proteins different from Gq/G11/G12/G13.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Developmental Biology - Volume 282, Issue 1, 1 June 2005, Pages 174-182
نویسندگان
, , , , ,