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. 2022 Mar 1;9:791094. doi: 10.3389/fmolb.2022.791094

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Copyright © 2022 Akiyama, Lyons, Fay, Tomioka, Abe, Anderson and Ivanov.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Involvement of other RNase A superfamily members than ANG in sodium arsenite (SA)-induced tRNA cleavage. (A) Northern blot analysis showing that SA treatment induces rRNA fragmentation but ANG does not. (B,C) SA treatment induces CCA-deactivated tRNAs even in ANG knockout (ΔANG) cells. (B) SYBR Gold staining and (C) Northern blotting of the CCA-specific ligation products. (D,E) RNH1 negatively regulates SA-induced tRNA cleavage. (D) SYBR Gold staining and (E) Northern blotting of the CCA-ligation products. Note that constitutive CCA-deactivation and tiRNA production are shown in RNH1 knockout (ΔRNH1) cells, and the amount of them was not increased by SA treatment. The blue arrowheads indicate the bands for pre-tRNAs.