Nonfunctional rRNA decay (NRD) is a quality control mechanism system capable of detecting and eliminating translationally defective rRNAs.
NRD can be divided into two pathways:
1) 18S NRD - eliminates rRNAs with deleterious mutations in the decoding site
2) 25S NRD - eliminates rRNAs containing deleterious mutations in the peptidyl transferase center
In contrast to 18S NRD, which is related to no-go mRNA decay, 25S NRD appears unrelated to any of the known translation-dependent mRNA decay pathways. Unlike NMD, NSD, NGD, and 18S NRD, 25S NRD still occurs in the presence of translation elongation inhibitors.
The ribosomal subunits that contain 25S NRD substrates fail to enter the translationally active pool. Once exported from the nucleus, 60S subunits undergo a number of cytoplasmic maturation steps involving the release of some nuclear acquired proteins and acquisition of cytoplasmic factors before becoming translationally competent. It is possible that 25S NRD is a consequence of the failure of one or more of these late maturation proteins to either efficiently bind or release newly synthesized 60S subunits containing an NRD substrate. Such late quality control steps could function to prevent 60S subunits with a functional defect in the peptidyl transferase center from interfering with normal protein synthesis. (PMID: 19481524)