Ionizing radiation (IR) causes DNA damage, particularly DNA double-strand breaks (DSBs), which have significant implications for genome stability. The major pathways of repairing DSBs are homologous recombination (HR) and nonhomologous end joining (NHEJ). However, the repair mechanism of IR-induced DSBs in embryos is not well understood, despite extensive research in somatic cells. The externally developing aquatic organism, Xenopus tropicalis, serves as a valuable model for studying embryo development. A significant increase in zygotic transcription occurs at the midblastula transition (MBT), resulting in a longer cell cycle and asynchronous cell divisions. This study examines the impact of X-ray irradiation on Xenopus embryos before and after the MBT. The findings reveal a heightened X-ray sensitivity in embryos prior to the MBT, indicating a distinct shift in the DNA repair pathway during embryo development. Importantly, we show a transition in the dominant DSB repair pathway from NHEJ to HR before and after the MBT. These results suggest that the MBT plays a crucial role in altering DSB repair mechanisms, thereby influencing the IR sensitivity of developing embryos.
Keyphrases
- dna repair
- dna damage
- radiation induced
- cell cycle
- cell free
- dna damage response
- oxidative stress
- high resolution
- cell proliferation
- induced apoptosis
- genome wide
- radiation therapy
- risk assessment
- cell therapy
- single molecule
- gene expression
- diabetic rats
- transcription factor
- signaling pathway
- pregnant women
- copy number
- computed tomography
- mesenchymal stem cells
- mass spectrometry
- electron microscopy