Ancient Sturgeons Possess Effective DNA Repair Mechanisms: Influence of Model Genotoxicants on Embryo Development of Sterlet, Acipenser ruthenus.

Ievgeniia Gazo,Ievgen Lebeda,Christoph Steinbach,Roman Franěk,Martin Pšenička,Radek Šindelka,Sahana Shivaramu

doi:10.3390/ijms22010006

Abstract

DNA damage caused by exogenous or endogenous factors is a common challenge for developing fish embryos. DNA damage repair (DDR) pathways help organisms minimize adverse effects of DNA alterations. In terms of DNA repair mechanisms, sturgeons represent a particularly interesting model due to their exceptional genome plasticity. Sterlet (Acipenser ruthenus) is a relatively small species of sturgeon. The goal of this study was to assess the sensitivity of sterlet embryos to model genotoxicants (camptothecin, etoposide, and benzo[a]pyrene), and to assess DDR responses. We assessed the effects of genotoxicants on embryo survival, hatching rate, DNA fragmentation, gene expression, and phosphorylation of H2AX and ATM kinase. Exposure of sterlet embryos to 1 µM benzo[a]pyrene induced low levels of DNA damage accompanied by ATM phosphorylation and xpc gene expression. Conversely, 20 µM etoposide exposure induced DNA damage without activation of known DDR pathways. Effects of 10 nM camptothecin on embryo development were stage-specific, with early stages, before gastrulation, being most sensitive. Overall, this study provides foundational information for future investigation of sterlet DDR pathways.

Highlights

DNA is subject to constant damage from endogenously produced reactive oxygen species that affect replication and transcription and can alter its structure [1]
Preliminary results showed that short-term exposure to BaP and etoposide at different stages had no effect on embryo viability or hatching rate
This study presents the first screening of DNA damage response pathways utilized by sterlet embryos

Summary

Introduction

DNA is subject to constant damage from endogenously produced reactive oxygen species that affect replication and transcription and can alter its structure [1]. Exogenous factors, such as radiation or pollutants, induce DNA damage via oxidation, DNA adduct formation, and single- or double-strand breaks (SSB or DSB, respectively). Cellular mechanisms for repair of DNA damage are highly conserved among vertebrates; species-specificity in processes and targets of DNA damage repair (DDR) are noted [2]. Cells initiate damage recognition and assembly of response complexes in response to DNA damage. An initial signal for DDR response is the phosphorylation of the histone

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