High-complexity of DNA double-strand breaks is key for alternative end-joining choice.

The repair of DNA double-strand breaks (DSBs) through alternative non-homologous end-joining (alt-NHEJ) pathway significantly contributes to genetic instability. However, the mechanism governing alt-NHEJ pathway choice, particularly its association with DSB complexity, remains elusive due to the absence of a suitable reporter system. In this study, we established a unique Escherichia coli reporter system for detecting complex DSB-initiated alternative end-joining (A-EJ), an alt-NHEJ-like pathway. By utilizing various types of ionizing radiation to generate DSBs with varying degrees of complexity, we discovered that high complexity of DSBs might be a determinant for A-EJ choice. To facilitate efficient repair of high-complexity DSBs, A-EJ employs distinct molecular patterns such as longer micro-homologous junctions and non-templated nucleotide addition. Furthermore, the A-EJ choice is modulated by the degree of homology near DSB loci, competing with homologous recombination machinery. These findings further enhance the understanding of A-EJ/alt-NHEJ pathway choice.

Activation of lipophagy ameliorates cadmium-induced neural tube defects via reducing low density lipoprotein cholesterol levels in mouse placentas.

Neural tube defects (NTDs) represent a prevalent and severe category of congenital anomalies in humans. Cadmium (Cd) is an environmental teratogen known to cause fetal NTDs. However, its underlying mechanisms remain elusive. This study aims to investigate the therapeutic potential of lipophagy in the treatment of NTDs, providing valuable insights for future strategies targeting lipophagy activation as a means to mitigate NTDs.We successfully modeled NTDs by Cd exposure during pregnancy. RNA sequencing was employed to investigate the transcriptomic alterations and functional enrichment of differentially expressed genes in NTD placental tissues. Subsequently, pharmacological/genetic (Atg5-/- placentas) experiments confirmed that inducing placental lipophagy can alleviate Cd induced-NTDs. We found that Cd exposure caused NTDs. Further analyzed transcriptomic data from the placentas with NTDs which revealed significant downregulation of low-density lipoprotein receptor associated protein 1(Lrp1) gene expression responsible for positive regulation of low-density lipoprotein cholesterol (LDL-C) transport. Correspondingly, there was an increase in maternal serum/placenta/amniotic fluid LDL-C content. Subsequently, we have discovered that Cd exposure activated placental lipophagy. Pharmacological/genetic (Atg5-/- placentas) experiments confirmed that inducing placental lipophagy can alleviate Cd induced-NTDs. Furthermore, our findings demonstrate that activation of placental lipophagy effectively counteracts the Cd-induced elevation in LDL-C levels. Lipophagy serves to mitigate Cd-induced NTDs by reducing LDL-C levels within mouse placentas.

IGF2BP3 prevent HMGB1 mRNA decay in bladder cancer and development.

BACKGROUND: IGF2BP3 functions as an RNA-binding protein (RBP) and plays a role in the posttranscriptional control of mRNA localization, stability, and translation. Its dysregulation is frequently associated with tumorigenesis across various cancer types. Nonetheless, our understanding of how the expression of the IGF2BP3 gene is regulated remains limited. The specific functions and underlying mechanisms of IGF2BP3, as well as the potential benefits of targeting it for therapeutic purposes in bladder cancer, are not yet well comprehended. METHODS: The mRNA and protein expression were examined by RT-qPCR and western blotting, respectively. The methylation level of CpG sites was detected by Bisulfite sequencing PCR (BSP). The regulation of IGF2BP3 expression by miR-320a-3p was analyzed by luciferase reporter assay. The functional role of IGF2BP3 was determined through proliferation, colony formation, wound healing, invasion assays, and xenograft mouse model. The regulation of HMGB1 by IGF2BP3 was investigated by RNA immunoprecipitation (RIP) and mRNA stability assays. RESULTS: We observed a significant elevation in IGF2BP3 levels within bladder cancer samples, correlating with more advanced stages and grades, as well as an unfavorable prognosis. Subsequent investigations revealed that the upregulation of IGF2BP3 expression is triggered by copy number gain/amplification and promoter hypomethylation in various tumor types, including bladder cancer. Furthermore, miR-320a-3p was identified as another negative regulator in bladder cancer. Functionally, the upregulation of IGF2BP3 expression exacerbated bladder cancer progression, including the proliferation, migration, and invasion of bladder cancer. Conversely, IGF2BP3 silencing produced the opposite effects. Moreover, IGF2BP3 expression positively correlated with inflammation and immune infiltration in bladder cancer. Mechanistically, IGF2BP3 enhanced mRNA stability and promoted the expression of HMGB1 by binding to its mRNA, which is a factor that promotes inflammation and orchestrates tumorigenesis in many cancers. Importantly, pharmacological inhibition of HMGB1 with glycyrrhizin, a specific HMGB1 inhibitor, effectively reversed the cancer-promoting effects of IGF2BP3 overexpression in bladder cancer. Furthermore, the relationship between HMGB1 mRNA and IGF2PB3 is also observed in mammalian embryonic development, with the expression of both genes gradually decreasing as embryonic development progresses. CONCLUSIONS: Our present study sheds light on the genetic and epigenetic mechanisms governing IGF2BP3 expression, underscoring the critical involvement of the IGF2BP3-HMGB1 axis in driving bladder cancer progression. Additionally, it advocates for the investigation of inhibiting IGF2BP3-HMGB1 as a viable therapeutic approach for treating bladder cancer.

Enhancement of Repeat-Mediated Deletion Rearrangement Induced by Particle Irradiation in a RecA-Dependent Manner in Escherichia coli.

Repeat-mediated deletion (RMD) rearrangement is a major source of genome instability and can be deleterious to the organism, whereby the intervening sequence between two repeats is deleted along with one of the repeats. RMD rearrangement is likely induced by DNA double-strand breaks (DSBs); however, it is unclear how the complexity of DSBs influences RMD rearrangement. Here, a transgenic Escherichia coli strain K12 MG1655 with a lacI repeat-controlled amp activation was used while taking advantage of particle irradiation, such as proton and carbon irradiation, to generate different complexities of DSBs. Our research confirmed the enhancement of RMD under proton and carbon irradiation and revealed a positive correlation between RMD enhancement and LET. In addition, RMD enhancement could be suppressed by an intermolecular homologous sequence, which was regulated by its composition and length. Meanwhile, RMD enhancement was significantly stimulated by exogenous λ-Red recombinase. Further results investigating its mechanisms showed that the enhancement of RMD, induced by particle irradiation, occurred in a RecA-dependent manner. Our finding has a significant impact on the understanding of RMD rearrangement and provides some clues for elucidating the repair process and possible outcomes of complex DNA damage.

TRIM29 hypermethylation drives esophageal cancer progression via suppression of ZNF750.

Esophageal cancer (ESCA) is the seventh most frequent and deadly neoplasm. Due to the lack of early diagnosis and high invasion/metastasis, the prognosis of ESCA remains very poor. Herein, we identify skin-related signatures as the most deficient signatures in invasive ESCA, which are regulated by the transcription factor ZNF750. Of note, we find that TRIM29 level strongly correlated with the expression of many genes in the skin-related signatures, including ZNF750. TRIM29 is significantly down-regulated due to hypermethylation of its promoter in both ESCA and precancerous lesions compared to normal tissues. Low TRIM29 expression and high methylation levels of its promoter are associated with malignant progression and poor clinical outcomes in ESCA patients. Functionally, TRIM29 overexpression markedly hinders proliferation, migration, invasion, and epithelial-mesenchymal transition of esophageal cancer cells, whereas opposing results are observed when TRIM29 is silenced in vitro. In addition, TRIM29 inhibits metastasis in vivo. Mechanistically, TRIM29 downregulation suppresses the expression of the tumor suppressor ZNF750 by activating the STAT3 signaling pathway. Overall, our study demonstrates that TRIM29 expression and its promoter methylation status could be potential early diagnostic and prognostic markers. It highlights the role of the TRIM29-ZNF750 signaling axis in modulating tumorigenesis and metastasis of esophageal cancer.

Investigation into the communication between unheated and heat-stressed Caenorhabditis elegans via volatile stress signals.

Our research group has recently found that radiation-induced airborne stress signals can be used for communication among Caenorhabditis elegans (C. elegans). This paper addresses the question of whether heat stress can also induce the emission of airborne stress signals to alert neighboring C. elegans and elicit their subsequent stress response. Here, we report that heat-stressed C. elegans produces volatile stress signals that trigger an increase in radiation resistance in neighboring unheated C. elegans. When several loss-of-function mutations affecting thermosensory neuron (AFD), heat shock factor-1, HSP-4, and small heat-shock proteins were used to test heat-stressed C. elegans, we found that the production of volatile stress signals was blocked, demonstrating that the heat shock response and ER pathway are involved in controlling the production of volatile stress signals. Our data further indicated that mutations affecting the DNA damage response (DDR) also inhibited the increase in radiation resistance in neighboring unheated C. elegans that might have received volatile stress signals, indicating that the DDR might contribute to radioadaptive responses induction by volatile stress signals. In addition, the regulatory pattern of signal production and action was preliminarily clarified. Together, the results of this study demonstrated that heat-stressed nematodes communicate with unheated nematodes via volatile stress signals.

ACAP1 Deficiency Predicts Inferior Immunotherapy Response in Solid Tumors.

BACKGROUND: ACAP1 plays a key role in endocytic recycling, which is essential for the normal function of lymphocytes. However, the expression and function of ACAP1 in lymphocytes have rarely been studied. METHODS: Large-scale genomic data, including multiple bulk RNA-sequencing datasets, single-cell sequencing datasets, and immunotherapy cohorts, were exploited to comprehensively characterize ACAP1 expression, regulation, and function. Gene set enrichment analysis (GSEA) was used to uncover the pathways associated with ACAP1 expression. Eight algorithms, including TIMER, CIBERSORT, CIBERSORT-ABS, QUANTISEQ, xCELL, MCPCOUNTER, EPIC, and TIDE, were applied to estimate the infiltrating level of immune cells. Western blotting, qPCR, and ChIP-PCR were used to validate the findings from bioinformatic analyses. A T-cell co-culture killing assay was used to investigate the function of ACAP1 in lymphocytes. RESULTS: ACAP1 was highly expressed in immune-related tissues and cells and minimally in other tissues. Moreover, single-cell sequencing analysis in tumor samples revealed that ACAP1 is expressed primarily in tumor-infiltrating lymphocytes (TILs), including T, B, and NK cells. ACAP1 expression is negatively regulated by promoter DNA methylation, with its promoter hypo-methylated in immune cells but hyper-methylated in other cells. Furthermore, SPI1 binds to the ACAP1 promoter and positively regulates its expression in immune cells. ACAP1 levels positively correlate with the infiltrating levels of TILs, especially CD8+ T cells, across a broad range of solid cancer types. ACAP1 deficiency is associated with poor prognosis and immunotherapeutic response in multiple cancer types treated with checkpoint blockade therapy (ICT). Functionally, the depletion of ACAP1 by RNA interference significantly impairs the T cell-mediated killing of tumor cells. CONCLUSIONS: Our study demonstrates that ACAP1 is essential for the normal function of TILs, and its deficiency indicates an immunologically "cold" status of tumors that are resistant to ICT.

A Non-Cell-Autonomous Mode of DNA Damage Response in Soma of Caenorhabditis elegans.

Life has evolved a mechanism called DNA damage response (DDR) to sense, signal and remove/repair DNA damage, and its deficiency and dysfunction usually lead to genomic instability and development of cancer. The signaling mode of the DDR has been believed to be of cell-autonomy. However, the paradigm is being shifted with in-depth research into model organism Caenorhabditis elegans. Here, we mainly investigate the effect of DDR activation on the radiosensitivity of vulva of C. elegans, and first found that the vulval radiosensitivity is mainly regulated by somatic DDR, rather than the DDR of germline. Subsequently, the worm lines with pharynx-specific rescue of DDR were constructed, and it is shown that the 9-1-1-ATR and MRN-ATM cascades in pharynx restore approximately 90% and 70% of vulval radiosensitivity, respectively, through distantly regulating the NHEJ repair of vulval cells. The results suggest that the signaling cascade of DDR might also operate in a non-cell autonomous mode. To further explore the underlying regulatory mechanisms, the cpr-4 mutated gene is introduced into the DDR-rescued worms, and CPR-4, a cysteine protease cathepsin B, is confirmed to mediate the inter-tissue and inter-individual regulation of DDR as a signaling molecule downstream of 9-1-1-ATR. Our findings throw some light on the regulation of DNA repair in soma of C. elegans, and might also provide new cues for cancer prevention and treatment.

Exposure of cyanobacterium Nostoc sp. to the Mars-like stratosphere environment.

During the HH-19-2 flight mission of the Chinese Scientific Experimental System, dried Nostoc sp. cells were exposed to the stratosphere environment (32,508 m altitude) for 3 h and 22 min. The atmospheric pressure, temperature, relative humidity, and ionizing and non-ionizing radiation levels at that altitude are similar to those on the surface of Mars. Although analyses revealed decreased photosynthetic activity, a decline in autofluorescence, and damage to the cellular morphology in the flight-exposed sample, the death rate was low (28%). Physiological changes were not obvious after the exposure to the Mars-like vacuum conditions. The ground-exposed samples showed a similar trend to the flight-exposed samples, but the damage was relatively slight. RNA-sequencing data revealed a number of affected metabolic pathways: photosynthetic system and CO2 fixation function, activation of antioxidant systems, heat shock protein, DNA repair, and protein synthesis. Results suggest that Nostoc sp. has the potential to survive in a Mars-like environment and that it may be a suitable pioneer species to colonize Mars in the future in closed life-support systems (base) or in localities with relatively suitable conditions for life, such as localities with water available.

Survival of desert algae Chlorella exposed to Mars-like near space environment.

Desert was considered terrestrial analogues of Mars. In this study, dried cells of desert green algae Chlorella were exposed to Mars-like near-space environment using high-altitude scientific balloons. We found that while a majority of Chlorella cells survived, they exhibited considerable damage, such as low photosynthetic activity, reduced cell growth, increased cell mortality rate, and altered chloroplast and mitochondrial ultrastructure. Additionally, transcriptome analysis of near space-exposed Chlorella cells revealed 3292 differentially expressed genes compared to cells in the control ground group, including heat shock proteins, antioxidant enzymes, DNA repair systems, as well as proteins related to the PSII apparatus and ribosomes. These data shed light on the possible survival strategy of desert algae to near space environments. Our results indicated that Mars-like near space conditions represent an extreme environment for desert algae in terms of temperature, pressure, and radiations. The survival strategy of Chlorella in response to near space will help gain insights into the possibility of extremophile colonization on the surface of Mars and in similar extraterrestrial habitats.

Enhancement of DNA damage repair potential in germ cells of Caenorhabditis elegans by a volatile signal from their irradiated partners.

Radiation-induced bystander effects have been demonstrated within organisms. Recently, it is found that the organisms can also signal irradiation cues to their co-cultured partners in a waterborne manner. In contrast, there is a limited understanding of radiation-induced airborne signaling between individuals, especially on the aspect of DNA damage responses (DDR). Here, we establish a co-culture experimental system using Caenorhabdis elegans in a top-bottom layout, where communication between "top" and "bottom" worms is airborne. The radiation response of top worms is evaluated using radio-adaptive response (RAR) of embryonic lethality (F1), which reflects an enhancement in repair potential of germ cells to subsequent DNA damage. It is shown that gamma-irradiation of bottom worms alleviates the embryonic lethality of top worms caused by 25 Gy of subsequent gamma-irradiation, i.e. RAR, indicating that a volatile signal might play an essential role in radiation-induced inter-worm communication. The RAR is absent in the top worms impaired in DNA damage checkpoint, nucleotide excision repair, and olfactory sensory neurons, respectively. The induction of RAR is restricted to the mitotic zone of the female germline of hermaphrodites. These results indicate that the top worms sense the volatile signal through cephalic sensory neurons, and the neural stimulation distantly modulates the DDR in germ mitotic cells, leading to the enhancement of DNA damage repair potential. The volatile signal is produced specifically by the L3-stage bottom worms and functionally distinct from the known sex pheromone. Its production and/or release are regulated by water-soluble ascaroside pheromones in a population-dependent manner.

Negative Modulation of Bystander DNA Repair Potential by X-Ray Targeted Tissue Volume in Arabidopsis thaliana.

Radiation-induced bystander effects (RIBE) entail a cascade of bystander signals produced by the hit cells to the neighboring cells to regulate various biological processes including DNA damage repair. However, there is little clarity regarding the effect of radiation-targeted volume (hit cell amount) on the DNA repair potential of the bystander cells. This is especially important to understand in the context of the whole organism, where the target usually consists of multiple types of cells/tissues. To address this question, model plant Arabidopsis thaliana was locally irradiated, and the DNA repair potential of bystander root-tip cells was assessed based on their radioresistance to subsequent high-dose radiation, i.e. radioadaptive responses (RAR). We found that X-ray irradiation of the aerial parts (AP) of A. thaliana seedlings (5 Gy) initiated RAR in the root-tip cells, which exhibited an alleviated repression of root growth and root cell division, and reduced amount of DNA strand breaks. We also observed an improvement in the repair efficiency of the homologous recombination (HR) and non-homologous end joining (NHEJ) pathways in the bystander root tip cells. We further expanded the X-ray targeted volume to include the aerial parts with upper parts of the primary root and compared it with X-ray irradiated aerial parts alone. Comparative analysis revealed that RAR for these end points either disappeared or decreased; specifically, the repair efficiency of HR was significantly reduced, indicating that radiation-targeted volume negatively modulates the bystander DNA repair potential. In contrast, X-ray irradiation of upper part of the primary root alone did not induce RAR of the root tip cells. Thus, we propose that additional X-ray irradiation of upper part of the primary root reduces the bystander DNA repair potential, possibly by selectively disturbing the transport of bystander signals responsible for HR repair.

A potential involvement of plant systemic response in initiating genotoxicity of Ag-nanoparticles in Arabidopsis thaliana.

The extensive availability of engineered nanomaterials in global markets has led to the release of substantial amounts of nanoparticles (NP) into atmosphere, water body and soil, yielding both beneficial and harmful effects in plant systems. The NP are mainly aggregated onto the surface of plant roots and leaves exposed and only slightly transported into other tissues with a low rate of internalization. This raises a question of whether plant systemic response is involved in the induction of biological effects of NP. To address this, model plant Arabidopsis thaliana were root exposed to low concentrations of Ag-NP of two particle sizes (10-nm and 60-nm), and expressions of homologous recombination (HR)-related genes and the alleviation of transcriptional gene silencing (TGS) in aerial leafy tissues were examined as genotoxic endpoints. Results showed that exposure of roots to two sizes of Ag-NP up-regulated expressions of HR genes, and reactivated TGS-silenced repetitive elements in aerial tissues. These effects were blocked by the impairment in the salicylic acid signal pathway, indicating a potential involvement of plant systemic response in the induction of Ag-NP genotoxicity. This is further supported by ICP-MS analysis, in which the Ag content in aerial tissues was not significantly changed by root exposure to 10-nm Ag-NP. Although a significant increase in the Ag content in aerial tissues was observed after root exposure to 60-nm Ag-NP, its genotoxic effects had no obvious difference from that by 10-nm Ag-NP exposure, also suggesting that the genotoxicity might be mainly induced via plant systemic response, at least in the experiments of root exposure to Ag-NP.

Cre-miR914-regulated RPL18 is involved with UV-B adaptation in Chlamydomonas reinhardtii.

UV radiation is a serious threat to life, and algae have developed highly efficient adaptations to UV radiation through the course of evolution. To date, studies investigating the mechanisms of UV adaptation in algae have focused on physiological regulation and associated protein coding genes, with only a few reports on associated protein non-coding genes. In a previous study, we found that Cre-miR914 was significantly down-regulated in Chlamydomonas reinhardtii in response to heat shock. In the present study, we aimed to determine whether Cre-miR914 plays a role in response to UV-B radiation. Our bioinformatics analysis indicated that the potential target gene of Cre-miR914 is ribosomal protein L18 (RPL18). We also measured the expression of Cre-miR914 and RPL18 in response to UV-B radiation through qPCR analysis. Then, we constructed cell lines overexpressing Cre-miR914 or RPL18, and performed survival experiments under UV-B stress. The results showed that Cre-miR914 overexpression decreased resistance while RPL18 overexpression enhanced tolerance to UV-B radiation. These results indicate that Cre-miR914 and its potential target gene RPL18 are involved in the adaptation to UV-B in C. reinhardtii.

Genotoxicity of Zinc Oxide Nanoparticles in Plants Demonstrated Using Transgenic Arabidopsis thaliana.

As important members of earth biosphere, higher plants are inevitably exposed to nanoparticles (NP) released into the environment. Therefore, determining NP-induced phytotoxicity is ecologically important. Currently, researches into genotoxic effects of NP on plants are limited. In this study, Arabidopsis thaliana lines transgenic for homologous recombination (HR) and transcriptional gene silencing (TGS) reporter genes were for the first time adopted to assess the genotoxicity of Zinc oxide NP (ZnO-NP). Results showed that the root exposure to ZnO-NP led to increased HR and alleviation of TGS in the aerial tissues, indicative of the genotoxicity of ZnO-NP in plants. The increased Zn content after root exposure to ZnO-NP and the similar induction of HR and TGS alleviation after root exposure to equivalent Zn ions suggested that the genotoxicity of ZnO-NP might be mainly induced by Zn ions in aerial tissues that were transported from decomposed ZnO-NP in either medium or plant roots.

Promoting Potato Seed Sprouting Using an Amphiphilic Nanocomposite.

Most potato tubers were used as seeds and sprouted relatively slowly in soil, greatly influencing potato production. To solve this problem, an amphiphilic nanocomposite was fabricated by loading hydrophobic silica (H-SiO2) in hydrophilic attapulgite nest-like and used as a nano presprouting agent (NPA). This technology could conveniently adjust the occupation area ratio of water and air (OARWA) on the potato surface. NPA could endow potatoes with an appropriate OARWA and, thus, effectively accelerate sprouting. Additionally, NPA greatly decreased soil bulk density, facilitated earthworm growth, promoted potato growth, and increased the yield by 14.1%. Besides, NPA did not pass through the potato skin and mainly existed on the surface of potatoes. Importantly, NPA showed tiny influence on the viability of fish and nematodes, demonstrating good biosafety. Therefore, this work provides a promising presprouting approach for potatoes, which may have a potential application prospect in ensuring food supply.

Sandwich-like Nanosystem for Simultaneous Removal of Cr(VI) and Cd(II) from Water and Soil.

In this work, a novel nanosystem with a sandwich-like structure was synthesized via face-to-face combination of two pieces of waste cotton fabrics (CFs) carrying ferrous sulfide (FeS) and carboxyl-functionalized ferroferric oxide microsphere (CFFM), respectively, and the obtained nanosystem was named as FeS/CFFM/CF. Therein, FeS has high reduction and adsorption capabilities for hexavalent chromium (Cr(VI)), CFFM possesses a high adsorption ability on cadmium ion (Cd(II)) through electrostatic attraction and chelation, and CF displays high immobilization ability for FeS and CFFM and adsorption performance on Cd(II). FeS/CFFM/CF could simultaneously remove Cr(VI) and Cd(II) from water and inhibit the uptake of Cr and Cd by fish and water spinach, ensuring the food safety. Besides, this technology could efficiently control the migration of Cr(VI) and Cd(II) in the sand-soil mixture, which was favorable to prevent their wide diffusion. Importantly, FeS/CFFM/CF possessed a high flexibility and could be conveniently produced with needed scale and shape and easily separated from water and soil, displaying a promising approach to remediate Cr(VI)-/Cd(II)-contaminated water and soil and a huge application potential.

Induction of reproductive cell death in Caenorhabditis elegans across entire linear-energy-transfer range of carbon-ion irradiation.

Heavy-ion radiation has attracted extensive attention as an effective cancer therapy because of the varying energy deposition along its track and its high cell-killing effect. Reproductive cell death (RCD), also known as clonogenic death, is an important mode of death of the cancer cells after radiotherapy. Although RCD induced by heavy-ion irradiation with various linear energy transfers has been demonstrated using clonogenic assay in vitro, little is known about the distribution of RCD across the range of heavy-ion irradiation at the level of whole organisms. In this study, a vulval tissue model of Caenorhabditis elegans was for the first time used to assess RCD in vivo induced by carbon-ion irradiation. A polymethyl methacrylate wedge was designed to provide a gradually varying thickness of shielding, so worms could be exposed to the entire range of carbon-ion irradiation. The carbon-ion irradiation led to a significant induction of RCD over the entire range in a dose-dependent manner. The biological peak did not correspond to the physical Bragg peak and moved forward, rather than spread forward, as radiation dose increased. The degree and shape of the range-distribution of RCD were also affected by the developmental stages of the worms. The gene mutations in DNA-damage checkpoints did not affect the responses of mutant worms positioned in biological peaks, compared to wild-type worms, but decreased radio-sensitivity in the entrance region. An increased induction of RCD was observed in the worms impaired in homologous recombination (HR), but not in non-homologous end jointing pathway, suggesting a crucial role of HR repair in vulval cells of C. elegans in dealing with the carbon-ion-induced DNA damage. These unique manifestations of RCD in vivo in response to carbon-ion irradiation might provide new clues for further investigating the biological effects of heavy-ion irradiation.

Effect of modeled microgravity on UV-C-induced interplant communication of Arabidopsis thaliana.

Controlled ecological life support systems (CELSS) will be an important feature of long-duration space missions of which higher plants are one of the indispensable components. Because of its pivotal role in enabling plants to cope with environmental stress, interplant communication might have important implications for the ecological stability of such CELSS. However, the manifestations of interplant communication in microgravity conditions have yet to be fully elucidated. To address this, a well-established Arabidopsis thaliana co-culture experimental system, in which UV-C-induced airborne interplant communication is evaluated by the alleviation of transcriptional gene silencing (TGS) in bystander plants, was placed in microgravity modeled by a two-dimensional rotating clinostat. Compared with plants under normal gravity, TGS alleviation in bystander plants was inhibited in microgravity. Moreover, TGS alleviation was also prevented when plants of the pgm-1 line, which are impaired in gravity sensing, were used in either the UV-C-irradiated or bystander group. In addition to the specific TGS-loci, interplant communication-shaped genome-wide DNA methylation in bystander plants was altered under microgravity conditions. These results indicate that interplant communications might be modified in microgravity. Time course analysis showed that microgravity interfered with both the production of communicative signals in UV-C-irradiated plants and the induction of epigenetic responses in bystander plants. This was further confirmed by the experimental finding that microgravity also prevented the response of bystander plants to exogenous methyl jasmonate (JA) and methyl salicylate (SA), two well-known airborne signaling molecules, and down-regulated JA and SA biosynthesis in UV-C-irradiated plants.