Abstract
Maintaining genomic stability is vital for cells as well as individual organisms. The meiotic recombination-related gene MRE11 (meiotic recombination 11) is essential for preserving genomic stability through its important roles in the resection of broken DNA ends, DNA damage response (DDR), DNA double-strand breaks (DSBs) repair, and telomere maintenance. The post-translational modifications (PTMs), such as phosphorylation, ubiquitination, and methylation, regulate directly the function of MRE11 and endow MRE11 with capabilities to respond to cellular processes in promptly, precisely, and with more diversified manners. Here in this paper, we focus primarily on the PTMs of MRE11 and their roles in DNA response and repair, maintenance of genomic stability, as well as their association with diseases such as cancer.
Highlights
Genetic information is faithfully transmitted from one cell to their progenies through its carrier DNA
Meiotic recombination 11 (MRE11) is phosphorylated at S676 by ribosomal S6 kinase (RSK), which disrupts MRE11 binding to DNA thereby blocks, ATM activation, and the phosphorylation of ATM’s downstream targets, NBS1 and H2AX [88]
MRE11 is arginine-methylated by PRMT1, and this methylation is required for intra-S-phase DNA damage checkpoint response [114]
Summary
Genetic information is faithfully transmitted from one cell to their progenies through its carrier DNA. Meiotic recombination 11 (MRE11), the key components of the MRE11-RAD50-NBS1 (MRN) complex which function mainly to activate ATM- or ATR-mediated DNA damage response (DDR) upon DNA damage [10], play important roles in processing broken DNA ends and mediating an essential step for repairing damaged DNA [10]. Plenty of somatic mutations (Table 1), including missense, frameshift and stop code gained, of genes encoded in the MRN complex have been linked to many types of cancer, such as breast, ovarian, colorectal, gastric, and prostate cancers [15]. All of these suggest that MRE11 and its copartners play vital roles in preventing genomic instability and tumorigenesis. We summarize the recent progress in the discovery of all PTMs on MRE11 and the contribution of these PTMs to the biological and molecular functions of MRE11, and provide new insights into the future research directions to the physiological and pathological processes of MRE11’s PTMs
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
