Impaired gametogenesis in mice that overexpress the RNA-binding protein HuR.
A series of experiments, using cell culture models or in vitro assays, has shown that the RNA-binding protein HuR increases the half-life of some messenger RNAs that contain adenylate/uridylate-rich decay elements. However, its function in an integrated system has not yet been investigated. Here, using a mouse model, we report that misregulation of HuR, due to expression of an HuR transgene, prevents the production of fully functional gametes. This work provides the first evidence for a physiological function of HuR, and highlights its involvement in spermatogenesis.
Levadoux-Martin
Marilyne
M
Centre de Biologie du Développement, CNRS, Université Paul Sabatier, Toulouse, France.
Gouble
Agnès
A
Jégou
Bernard
B
Vallet-Erdtmann
Virginie
V
Auriol
Jacques
J
Mercier
Pascale
P
Morello
Dominique
D
D000818:Animals; D030801:Animals, Genetically Modified; D000954:Antigens, Surface; D003433:Crosses, Genetic; D051959:ELAV Proteins; D000067780:ELAV-Like Protein 1; D005260:Female; D018703:Founder Effect; D005718:Gametogenesis / Q000235:genetics*; D005786:Gene Expression Regulation; D006801:Humans; D008297:Male; D051379:Mice; D016601:RNA-Binding Proteins / Q000235:genetics*
D000954:Antigens, Surface; D051959:ELAV Proteins; D000067780:ELAV-Like Protein 1; C098770:ELAVL1 protein, human; D016601:RNA-Binding Proteins