z-logo
open-access-imgOpen Access
tRNA cleavage: a new insight
Author(s) -
Sherif Rashad,
Kuniyasu Niizuma,
Teiji Tominaga
Publication year - 2020
Publication title -
neural regeneration research/neural regeneration research
Language(s) - Uncategorized
Resource type - Journals
SCImago Journal Rank - 0.93
H-Index - 38
eISSN - 1876-7958
pISSN - 1673-5374
DOI - 10.4103/1673-5374.264447
Subject(s) - transfer rna , cleavage (geology) , rna , angiogenin , biology , microbiology and biotechnology , protein biosynthesis , ribosome , mitochondrion , biochemistry , chemistry , genetics , gene , paleontology , fracture (geology) , angiogenesis
Over the past decades, tRNA was found to be a rich hub of RNA modifications such as 1-methyladenosine and 5-methycytosine modifications and others, holding more than half of all modifications occurring in RNA molecules. Moreover, tRNA was discovered to be a source of various small noncoding RNA species, such as the stress induced angiogenin cleaved tRNA halves (tiRNA) or the miRNA like tRNA derived fragments. tRNA cleavage under stress was fist discovered in bacteria and later was found to be conserved across different species, including mammals. Under cellular stress conditions, tRNA undergoes conformational changes and angiogenin cleaves it into 3' and 5' halves. 5'tiRNA halves were shown to repress protein translations. tRNA cleavage is thought of to be a cytoprotective mechanism by which cells evade apoptosis, however some data hints to the opposite; that tiRNA are cytotoxic or at least related to apoptosis initiation. tRNA cleavage also was shown to be affected by tRNA modifications via different enzymes in the cytosol and mitochondria. In this review, we will highlight the biology of tRNA cleavage, show the evidence of it being cytoprotective or a marker of cell death and shed a light on its role in disease models and human diseases as well as possible future directions in this field of RNA research.

The content you want is available to Zendy users.

Already have an account? Click here to sign in.
Having issues? You can contact us here