Leishmaniasis and trypanosomiasis are largely neglected diseases prevailing in tropical and subtropical conditions. These are an arthropod-borne zoonosis that affects humans and some animals and is caused by infection with protozoan of the genera Leishmania and Trypanosoma, respectively. These parasites present high genomic plasticity and are able to adapt themselves to adverse conditions like the attack of host cells or toxicity induced by drug exposure. Different mechanisms allow these adapting responses induced by stress, such as mutation, chromosomal rearrangements, establishment of mosaic ploidies, and gene expansion. Here we describe how a subset of genes encoding for DNA polymerases implied in repairing/translesion (TLS) synthesis are duplicated in some pathogenic species of the Trypanosomatida order and a free-living species from the Bodonida order. These enzymes are both able to repair DNA, but are also error-prone under certain situations. We discuss about the possibility that these enzymes can act as a source of genomic variation promoting adaptation in trypanosomatids.

利什曼病和锥虫病是热带和亚热带地区普遍被忽视的疾病。这些是节肢动物传播的人畜共患病，影响人类和某些动物，是由该属原生动物感染引起的利什曼原虫 和 锥虫， 分别。这些寄生虫具有很高的基因组可塑性，能够适应不利条件，例如宿主细胞的攻击或药物暴露引起的毒性。不同的机制允许这些由应激诱导的适应性反应，例如突变，染色体重排，镶嵌倍数的建立和基因扩增。在这里，我们描述了在Trypanosomatida阶的某些致病物种和Bodonida阶的自由生活物种中如何复制在修复/转运（TLS）合成中暗含的编码DNA聚合酶的基因子集。这些酶既能够修复DNA，又在某些情况下容易出错。我们讨论了有关这些酶可以充当基因组变异的来源的可能性，从而促进锥虫的适应性。