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. Author manuscript; available in PMC: 2021 Jan 7.
Published in final edited form as: Cell Rep. 2020 Dec 22;33(12):108527. doi: 10.1016/j.celrep.2020.108527

Figure 7. Model for Operon Activation.

Figure 7.

(A) In ΔtruA strains, hypomodified tRNAs are susceptible to nuclease, leading to tRNA fragment accumulation. RtcA converts the ends of the 5′ fragments to 2′, 3′-cyclic phosphate (cP).

(B) In ΔruvA strains and after treatment with DNA damaging agents, a RecA-regulated endonuclease cleaves tRNAs, resulting in 5′ halves ending in cyclic phosphate.

(C–E) We propose that 5′ tRNA halves ending in cyclic phosphate can be degraded by PNPase (C); bind the CARF domain of a RtcR dimer, resulting in oligomerization and operon activation (D); and may also be repaired by RtcB (E).