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Cullin-RING ligases (CRLs) complexes participate in the regulation of diverse cellular processes, including cell cycle progression, transcription, signal transduction and development. Serving as the scaffold protein, cullins are crucial for the assembly of ligase complexes, which recognize and target various substrates for proteosomal degradation. Mutations in human  CUL4B , one of the eight members in cullin family, are one of the major causes of X-linked mental retardation. We here report the generation and characterization of  Cul4b  knockout mice, in which exons 3 to 5 were deleted. In contrast to the survival to adulthood of human hemizygous males with  CUL4B  null mutation,  Cul4b  null mouse embryos show severe developmental arrest and usually die before embryonic day 9.5 (E9.5). Accumulation of cyclin E, a CRL (CUL4B) substrate, was observed in  Cul4b  null embryos.  Cul4b  heterozygotes were recovered at a reduced ratio and exhibited a severe developmental delay. The placentas in  Cul4b  heterozygotes were disorganized and were impaired in vascularization, which may contribute to the developmental delay. As in human  CUL4B  heterozygotes,  Cul4b  null cells were selected against in  Cul4b  heterozygotes, leading to various degrees of skewed X-inactivation in different tissues. Together, our results showed that CUL4B is indispensable for embryonic development in the mouse.

Lack of Cul4b, an E3 Ubiquitin Ligase Component, Leads to Embryonic Lethality and Abnormal Placental Development