Jujube (Ziziphus jujuba Mill.) is a fruit tree that is gaining increasing importance in drought-affected regions worldwide. The fruit size is an important quantitative agronomic trait that affects not only the fruit yield and attractiveness but also consumer preference. Genetic enhancement of fruit appearance is a fundamental goal of jujube breeding programs. The genetic control of jujube fruit size traits is highly quantitative, and development of high-density genetic maps can facilitate fine mapping of quantitative trait loci (QTLs) and gene identification. However, studies regarding the construction of high-density molecular linkage maps and identification of quantitative trait loci (QTLs) targeting fruit size in jujube are limited. In this study, we performed whole-genome resequencing of the jujube cultivars “JMS2” and “Xing16” and their 165 F₁ progenies to identify genome-wide single-nucleotide polymorphism (SNP) markers and constructed a high-density bin map of jujube that can be used to assist in the selection of multiple traits in jujube breeding. This analysis yielded a total of 116,312 SNPs and a genetic bin map of 2398 bin markers spanning 1074.33 cM with an average adjacent interval of 0.45 cM. A quantitative genetic analysis identified 15 QTLs related to fruit size and the observed phenotypic variation associated with a single QTL ranged from 9.5 to 13.3%. Through the screening of overlapping and stable QTL regions, we identified 113 candidate genes related to fruit size. These genes were ascertained to be involved in cell division, cell wall metabolism, synthesis of phytohormones (ABA, IAA, and auxin), and encoding of enzymes and transcription factors. These candidate genomic regions will facilitate marker-assisted breeding of fruits with different sizes and shapes and lay a foundation for future breeding and manipulation of fruit size and shape in jujube.

Fluopyram, a SDH inhibitor fungicide, is widely used in agriculture to control fungi and nematodes. However, fluopyram has been proved toxic that caused damage to organs through oxidative stress. The development of natural extracts that can reduce oxidative damage is a promising method. Lentinan is isolated from Lentinus edodes and has been verified its antioxidant activity. In this study, Caenorhabditis elegans was used to evaluate the protective effects of lentinan against fluopyram-induced toxicity and the possible mechanisms. Results showed that lentinan pretreatment notably increased the survival rate of N2 nematodes by 15.0 % and extended the lifespan by 91.5 %, compared with the fluopyram treatment. Lentinan pretreatment reverted the inhibition of the locomotion and reproduction of C. elegans under the fluopyram stress. In addition, lentinan pretreatment significantly decreased the contents of ROS and MDA in N2 nematodes. Moreover, pretreated with lentinan significantly recovered the decreased activities of CAT, SOD, GST and SDH induced by fluopyram. Lentinan pretreatment enhanced the mRNA levels of daf-16 and skn-1 and their downstream genes in the nematodes compared with the fluopyram group. In daf-16 and skn-1 mutants, the lifespan, ROS and related genes expression were not significantly changed in lentinan pretreatment. Pretreated with lentinan significantly enhanced the fluorescence intensity of SOD-3::GFP and GST-4::GFP, and promoted the nuclear translocation of DAF-16 and SKN-1 under the fluopyram stress. In summary, these findings indicated that lentinan protected C. elegans from fluopyram-induced toxicity via DAF-16 and SKN-1.

Salt stress is one of the main abiotic stresses that affects peach growth. Hydrogen sulfide has an important role in regulating plant resistance to salt stress. However, the mechanism by which hydrogen sulfide regulates salt stress resistance is currently unclear in peach. Here, we investigated the mechanism by which hydrogen sulfide alleviates salt stress in peach trees. In our study, exogenous hydrogen sulfide enhances the activity of antioxidant enzymes and reduces the accumulation of reactive oxygen species, thereby mitigating salt stress damage to seedlings. Moreover, transcriptome analysis was carried out and an encoding allene oxide synthase gene (AOS), PpAOS3, which is highly responsive to hydrogen sulfide, was found. Overexpression of PpAOS3 increased the root length and jasmonic acid (JA) content and attenuated growth inhibition under salt stress in Arabidopsis. NBT and Evans staining showed that Arabidopsis overexpressing PpAOS3 reduces O²⁻ accumulation and cell death under salt stress. Additionally, transcriptome analysis revealed that 10 genes encoding oxidoreductase were upregulated after hydrogen sulfide treatment. RT-qPCR was also performed which showed that these genes were upregulated to different degrees after hydrogen sulfide treatment. In conclusion, a hydrogen-sulfide-mediated PpAOS3-JA module significantly contributes to salt resistance in peach. These results can serve as a theoretical basis for utilizing hydrogen sulfide to improve the salt tolerance of peach.

Fluopimomide is a new pesticide that is widely applied in agriculture; however, the effects and molecular mechanisms of fluopimomide in inhibiting nematode reproduction remain unknown. In this study, the effects of fluopimomide on the development and infection of Meloidogyne incognita and the reproductive toxicity in Caenorhabditis elegans were evaluated. Results showed that, in comparison to inoculated control, fluopimomide at 0.33, 0.67, and 1.0 mg/kg soil significantly (p < 0.05) delayed M. incognita development and decreased the reproduction in pot experiments. Fluopimomide notably reduced the galls index with a control effect of 78.6%, 67.9%, and 50.0%, respectively. In addition, a dose–response relationship existed between the brood size and germ cell number of C. elegans and fluopimomide concentrations. Compared with the control group, fluopimomide at 1.0 and 5.0 mg/L notably (p < 0.001) increased the number of cell corpses per gonad in the N2 strain of C. elegans by 8.8- and 14.4-fold, respectively. The number of cell corpses per gonad was similar between the fluopimomide treated worms and the control group in mutants of ced-3, ced-4, and ced-9. Further evidence revealed fluopimomide significantly enhanced the expression of cep-1, egl-1, and clk-2, while no obvious effects were observed in their mutants. Taken together, these results indicated that fluopimomide inflicted DNA damage and induced the core apoptosis pathway caused by germ-cell apoptosis, leading to the reduction of the brood size of C. elegans.