Inactivation of ribosomal protein S27-like confers radiosensitivity via the Mdm2-p53 and Mdm2–MRN–ATM axes View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2018-02-02

AUTHORS

Yongchao Zhao, Mingjia Tan, Xia Liu, Xiufang Xiong, Yi Sun

ABSTRACT

RPS27L (ribosomal protein S27-like) is an evolutionarily conserved ribosomal protein and a direct p53 target. We recently reported that Rps27l disruption triggers ribosomal stress to induce p53, causing postnatal death, which can be rescued by Trp53+/−. Whether and how Rps27l modulates radiosensitivity is unknown. Here we report that Rps27l−/−; Trp53+/− mice are extremely sensitive to radiation due to reduced proliferation and massive induction of apoptosis in radiation-sensitive organs. Mechanistically, the radiation sensitivity is mediated by two signaling pathways: (1) activated p53 pathway due to imbalanced Mdm2/Mdm4 levels and reduced E3 ligase activity; and (2) reduced DNA damage response due to reduced MRN/Atm signal as a result of elevated Mdm2 binding of Nbs1 to inhibit Nbs1–Atm binding and subsequent Atm activation. Indeed, heterozygous deletion of Mdm2 restores the MRN/Atm signal. Collectively, our study revealed a physiological condition under which Rps27l regulates the Mdm2/p53 and MRN/Atm axes to maintain DNA damage response and to confer radioprotection in vivo. More... »

PAGES

145

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/s41419-017-0192-3

DOI

http://dx.doi.org/10.1038/s41419-017-0192-3

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1100774471

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/29396424


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