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. 2023 Jan 26;13:1102462. doi: 10.3389/fcimb.2023.1102462

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Copyright © 2023 Black, Reis-Cunha, Cruz and Tosi

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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Control over genome plasticity in Leishmania is multifactorial. Numerous processes are thought to contribute to Leishmania genome plasticity. (A) Inherent DNA instability may be a key source of genome plasticity events in Leishmania. How these events are repaired and/or tolerated may offer deeper insights into how they are exploited by Leishmania. (B) By increasing or decreasing the abundance of extrachromosomal amplicons, Leishmania can modulate the corresponding mRNA levels in response to changing environments. (C) Epistatic interactions may operate in Leishmania, allowing compensatory mutations or genomic rearrangements to arise. (D) The putative regulation of translation by non-coding RNAs may permit the modulation of translation efficiency.