Puente-Rivera Jonathan, Flores-Vega José Jesús, Morales-Reyna Marcos, Figueroa-Angulo Elisa Elvira, Pérez-Navarro Yussel, Salgado-Aguayo Alfonso, Carlos-Reyes Ángeles, Alvarez-Sánchez Maria Elizbeth
Laboratorio de Patogénesis Celular y Molecular Humana y Veterinaria, Posgrado en Ciencias Genómicas, Universidad Autónoma de la Ciudad de México (UACM), San Lorenzo 290, Col. Del Valle, Ciudad de México 03100, Mexico.
División de Investigación, Hospital Juárez de México, Instituto Politécnico Nacional 5160, Col. Magdalena de las Salinas, Ciudad de México 07760, Mexico.
Pathogens. 2025 Jun 5;14(6):565. doi: 10.3390/pathogens14060565.
, the protozoan responsible for trichomoniasis, encounters fluctuating levels of metal cations in the male urogenital tract, notably zinc (Zn) and cadmium (Cd), which may induce genotoxic stress. While zinc is a key physiological component of the male reproductive tract, both Zn and Cd can become genotoxic at elevated concentrations. However, their effect on DNA repair mechanisms in remains poorly understood. This study characterizes, for the first time, the expression and modulation of the recombinase TvRAD51, a homologous recombination (HR) key enzyme, in response to UV irradiation and sublethal concentrations of Zn (1.6 mM) and Cd (0.1 mM). In silico analyses confirmed the presence and conserved structure of the tvrad51 gene and its interaction with HR-related proteins, such as TvBLM and TvBRCA2. Quantitative RT-PCR, Western blot, and immunofluorescence assays revealed that TvRAD51 is upregulated at both transcript and protein levels following UV- and cation-induced DNA damage, with distinct temporal expression patterns for Zn and Cd exposure. Notably, TvRAD51 showed nuclear localization at early time points post-exposure, suggesting active participation in DNA repair processes. These findings demonstrate that TvRAD51 is a central component of the genotoxic stress response in , potentially contributing to parasite survival and adaptation in hostile environments through homologous recombination repair pathways.
导致滴虫病的原生动物在男性泌尿生殖道中会遇到金属阳离子水平的波动,尤其是锌(Zn)和镉(Cd),这可能会诱导基因毒性应激。虽然锌是男性生殖道的关键生理成分,但锌和镉在高浓度时都可能具有基因毒性。然而,它们对[滴虫名称未给出]DNA修复机制的影响仍知之甚少。本研究首次表征了重组酶TvRAD51(一种同源重组(HR)关键酶)在响应紫外线照射以及亚致死浓度的锌(1.6 mM)和镉(0.1 mM)时的表达和调控情况。计算机分析证实了tvrad51基因的存在及其保守结构,以及它与HR相关蛋白(如TvBLM和TvBRCA2)的相互作用。定量逆转录聚合酶链反应、蛋白质免疫印迹和免疫荧光分析表明,在紫外线和阳离子诱导的DNA损伤后,TvRAD51在转录本和蛋白质水平均上调,锌和镉暴露后的时间表达模式不同。值得注意的是,TvRAD51在暴露后的早期时间点显示出核定位,表明其积极参与DNA修复过程。这些发现表明,TvRAD51是[滴虫名称未给出]基因毒性应激反应的核心成分,可能通过同源重组修复途径有助于寄生虫在恶劣环境中的存活和适应。