The PARN, TOE1, and USB1 RNA deadenylases and their roles in non-coding RNA regulation

• Published in: The Journal of biological chemistry Vol. 299; no. 9; p. 105139
• Main Authors: Huynh, Thao Ngoc, Parker, Roy
• Format: Journal Article
• Language: English
• Published: United States Elsevier Inc 01.09.2023; American Society for Biochemistry and Molecular Biology
• Subjects: deadenylases; JBC Reviews; non-coding RNA regulation; PARN; TOE1; USB1; TOE1; non-coding RNA regulation; scaRNAs; snoRNAs; hTR; PCH7; PARN; USB1; deadenylases; ncRNA; RRM; snRNA; PABPs; TTP; NLS; PCH; BMF; IPF; DC
• ISSN: 0021-9258; 1083-351X
• DOI: 10.1016/j.jbc.2023.105139

The levels of non-coding RNAs (ncRNAs) are regulated by transcription, RNA processing, and RNA degradation pathways. One mechanism for the degradation of ncRNAs involves the addition of oligo(A) tails by non-canonical poly(A) polymerases, which then recruit processive sequence-independent 3′ to 5′ exonucleases for RNA degradation. This pathway of decay is also regulated by three 3′ to 5′ exoribonucleases, USB1, PARN, and TOE1, which remove oligo(A) tails and thereby can protect ncRNAs from decay in a manner analogous to the deubiquitination of proteins. Loss-of-function mutations in these genes lead to premature degradation of some ncRNAs and lead to specific human diseases such as Poikiloderma with Neutropenia (PN) for USB1, Dyskeratosis Congenita (DC) for PARN and Pontocerebellar Hypoplasia type 7 (PCH7) for TOE1. Herein, we review the biochemical properties of USB1, PARN, and TOE1, how they modulate ncRNA levels, and their roles in human diseases.