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In vivo function of CDK5 and Abl enzyme substrate 2 (Cables2), belonging to the Cables protein family, is unknown. Here, we found that targeted disruption of the entire  Cables2  locus ( Cables2d ) caused growth retardation and enhanced apoptosis at the gastrulation stage and then induced embryonic lethality in mice. Comparative transcriptome analysis revealed disruption of  Cables2 , 50% down-regulation of  Rps21  abutting on the  Cables2  locus, and up-regulation of p53-target genes in  Cables2d  gastrulas. We further revealed the lethality phenotype in  Rps21 -deleted mice and unexpectedly, the exon 1-deleted  Cables2  mice survived. Interestingly, chimeric mice derived from  Cables2d  ESCs carrying exogenous  Cables2  and tetraploid wild-type embryo overcame gastrulation. These results suggest that the diminished expression of  Rps21  and the completed lack of  Cables2  expression are intricately involved in the embryonic lethality via the p53 pathway. This study sheds light on the importance of  Cables2  locus in mouse embryonic development.

Disruption of entire Cables2 locus leads to embryonic lethality by diminished Rps21 gene expression and enhanced p53 pathway