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RACK1 depletion in a mouse model causes lethality, pigmentation deficits and reduction in protein synthesis efficiency
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RACK1 depletion in a mouse model causes lethality, pigmentation deficits and reduction in protein synthesis efficiency
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Journal Article
RACK1 depletion in a mouse model causes lethality, pigmentation deficits and reduction in protein synthesis efficiency
2013
Overview
The receptor for activated C-kinase 1 (RACK1) is a conserved structural protein of 40S ribosomes. Strikingly, deletion of RACK1 in yeast homolog Asc1 is not lethal. Mammalian RACK1 also interacts with many nonribosomal proteins, hinting at several extraribosomal functions. A knockout mouse for RACK1 has not previously been described. We produced the first RACK1 mutant mouse, in which both alleles of RACK1 gene are defective in RACK1 expression (ΔF/ΔF), in a pure C57 Black/6 background. In a sample of 287 pups, we observed no ΔF/ΔF mice (72 expected). Dissection and genotyping of embryos at various stages showed that lethality occurs at gastrulation. Heterozygotes (ΔF/+) have skin pigmentation defects with a white belly spot and hypopigmented tail and paws. ΔF/+ have a transient growth deficit (shown by measuring pup size at P11). The pigmentation deficit is partly reverted by p53 deletion, whereas the lethality is not. ΔF/+ livers have mild accumulation of inactive 80S ribosomal subunits by polysomal profile analysis. In ΔF/+ fibroblasts, protein synthesis response to extracellular and pharmacological stimuli is reduced. These results highlight the role of RACK1 as a ribosomal protein converging signaling to the translational apparatus.
Publisher
SP Birkhäuser Verlag Basel,Springer Nature B.V
Subject
/ Biomedical and Life Sciences
/ Deletion
/ Embryo, Mammalian - metabolism
/ Embryo, Mammalian - ultrastructure
/ Embryos
/ Humans
/ Kinases
/ Mice
/ Proteins
/ Receptors for Activated C Kinase
/ RNA, Small Interfering - genetics
/ Rodents
/ Tumor Suppressor Protein p53 - genetics
/ Tumor Suppressor Protein p53 - metabolism
/ Yeast
