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Radiation mutation breeding has been used for nearly 100 years and has successfully improved crops by increasing genetic variation. Global food production is facing a series of challenges, such as rapid population growth, environmental pollution and climate change. How to feed the world's enormous human population poses great challenges to breeders. Although advanced technologies, such as gene editing, have provided effective ways to breed varieties, by editing a single or multiple specific target genes, enhancing germplasm diversity through mutation is still indispensable in modern and classical radiation breeding because it is more likely to produce random mutations in the whole genome. In this short review, the current status of classical radiation, accelerated particle and space radiation mutation breeding is discussed, and the molecular mechanisms of radiation-induced mutation are demonstrated. This review also looks into the future development of radiation mutation breeding, hoping to deepen our understanding and provide new vitality for the further development of radiation mutation breeding.

Clustered DNA damage is considered as a critical type of lesions induced by ionizing radiation, which can be converted into the fatal or strong mutagenic complex double strand breaks (DSBs) during damage processing in the cells. The new data show that high energy protons produce more potentially lethal DSBs than low LET radiation. In this study, plasmid DNA were used to investigate and re-evaluate the biological effects induced by the protons with the LET of ~3.6 keV/μm at the molecular level in vitro, including single strand breaks (SSBs), DSBs, isolated and clustered base damages. The results of complex DNA damage detections indicated that protons at the given LET value induce about 1.6 fold more non-DSB clustered DNA damages than the prompt DSB. The DNA damage yields by protons were greater than that by γ-rays, specifically by 6 fold for the isolated type of DNA damage and 14 fold for the clustered damage. Furthermore, the spectrum of damages was also demonstrated to be depended on the radiation quality, with protons producing more DSBs relative to clusters than do γ-rays. In the space radiation field, the primary components are galactic cosmic rays (GCR) and solar particle events (SPE). GCR particles consist of 87% protons, 12% alpha particles and about 1% of heavy ions. SPE particles are mainly protons. Among these, protons are obviously the most abundant type of charged particles [1]. Model calculations have suggested that, during transit to Mars, every cell in an astronaut's body would be hit by a proton every few days [2,3]. On earth, worldwide over 40000 cancer patients have received proton radiotherapy [4]. The increasing use of proton radiotherapy necessitates strengthening the study of the basic biological mechanisms associated with exposure to protons. In generally, protons are classified as low linear energy transfer (LET) like the photon from X and γ-rays, that is to say they do not lose much energy when they pass through the matter. DNA is one of the most important targets of ionizing radiation, and the double-strand breakage (DSB) is a particularly hazardous type of DNA damage to dividing cells as it involves a break to both strands nearby in the double helix [5]. The data of Hada and Sutherland [6] indicate that high energy (1 GeV/nucleon, 0.22 keV/μm) protons produce more potentially lethal double-strand breaks (DSBs) than low LET radiation, and the spectrum of damages is very similar to that of high energy iron ions and other heavy charged particles. The distinctive biological mark of heavy ions with high LET is to induce complex DNA damage, including DSBs and non-DSB clustered DNA damage. Clustered lesions are defined as two or more lesions (base damage, single strand break, abasic site) formed within a ~10-bp segment by a single radiation track. Both DSBs and non-DSB clustered DNA damages are considered difficult to be repaired and are closely associated with mutations and cell death. So for re-evaluating the effects of protons on biological systems, it is important to further investigate t...

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Proton radiation (PR) and microgravity (μG) are two key factors that impact living things in space. This study aimed to explore the combined effects of PR and simulated μG (SμG) on bone function. Mouse embryo osteoblast precursor cells (MC3T3-E1) were irradiated with proton beams and immediately treated with SμG for 2 days using a three-dimensional clinostat. All samples were subjected to cell viability, alkaline phosphatase (ALP) activity and transcriptome assays. The results showed that cell viability decreased with increasing doses of PR. The peak ALP activity after PR or SμG alone was lower than that obtained with the non-treatment control. No difference in cell viability or ALP activity was found between 1 Gy PR combined with SμG (PR-SμG) and PR alone. However, 4 Gy PR-SμG resulted in decreased cell viability and ALP activity compared with those obtained with PR alone. Furthermore, Gene Ontology analysis revealed the same trend. These results revealed that PR-SμG may lead to reductions in the proliferation and differentiation capacities of cells in a dose-dependent manner. Our data provide new insights into bone-related hazards caused by multiple factors, such as PR and μG, in the space environment.