Strawberry anthracnose caused by Colletotrichum spp. is one of the most serious diseases in the strawberry fields of China. In total, 196 isolates of Colletotrichum were obtained from leaves, stolons, and crowns of strawberry plants with anthracnose symptoms in eastern China and were characterized based on morphology, internal transcribed spacer (ITS), and β-tubulin (TUB2) gene sequences. All 196 isolates were identified as the Colletotrichum gloeosporioides species complex. In total, 62 strains were further identified at the species level by phylogenetic analyses of multilocus sequences of ITS, glyceraldehyde-3-phosphate dehydrogenase (GAPDH), actin (ACT), Apn2-Mat1-2 intergenic spacer and partial mating type (ApMat), calmodulin (CAL), and TUB2. Three species from the C. gloeosporioides species complex were identified: Colletotrichum siamense, C. fructicola, and C. aenigma. Isolates of C. siamense were tolerant to high temperatures, with a significantly larger colony diameter than the other two species when grown above 36°C. The inoculation of strawberry plants confirmed the pathogenicity of all three species. C. siamense isolates resulted in the highest disease severity. The in vitro sensitivities of C. siamense and C. fructicola isolates to azoxystrobin and three demethylation-inhibitor (DMI) fungicides (difenoconazole, tebuconazole, and prochloraz) were determined. Both species were sensitive to DMI fungicides but not to azoxystrobin. C. siamense isolates were more sensitive to prochloraz, while C. fructicola isolates were more sensitive to difenoconazole and tebuconazole. The present study provides valuable information for the effective management of strawberry anthracnose.

In order to address the global crisis in pear productivity, there has been increased attention given to advocating for the use of organic fertilizers. As part of this effort, researchers have been investigating the microbial properties of organic fertilizers to better understand their potential impact on fruit productivity. Our research focused specifically on the impact of four different ratios of sheep manure (SM) and chemical fertilizers (CF) on pear productivity. We found that replacing CF with SM resulted in a proliferation of gammaproteobacteria, Chlamydiae, Bastocatellia and Clostridia in the soil rhizosphere, which is the region around the roots of plants where most nutrient uptake occurs. Using redundancy analysis, we were able to determine that SM was particularly effective at promoting the growth of gammaproteobacteria and clostridia, which were associated with C:N ratios around 14:1 as well as the availability of K, Fe, Zn and Cu. This combination of factors was conducive to a transition from vegetative growth to reproductive growth, resulting in an increase in pear production from 43 to 56 tons per hectare. We also discovered that Blastociella acts as a buffering system in regulating soil acidity. Taken together, our findings indicate that a combination of SM and CF can improve the abundance of beneficial bacteria in the rhizosphere, leading to an increase in pear productivity.

The receptor-like kinase SIT1 acts as a sensor in rice (Oryza sativa) roots, relaying salt stress signals via elevated kinase activity to enhance salt sensitivity. Here, we demonstrate that Protein Phosphatase 2A (PP2A) regulatory subunit B9κ constrains SIT1 activity under salt stress. B9κ-PP2A deactivates SIT1 directly by dephosphorylating the kinase at Thr515/516, a salt-induced phosphorylation site in the activation loop that is essential for SIT1 activity. B9κ overexpression suppresses the salt sensitivity of rice plants expressing high levels of SIT1, thereby contributing to salt tolerance. B9κ functions in a SIT1 kinase-dependent manner. During early salt stress, activated SIT1 phosphorylates B9κ; this not only enhances its binding with SIT1, it also promotes B9κ protein accumulation via Ser502 phosphorylation. Consequently, by blocking SIT1 phosphorylation, B9κ inhibits and fine-tunes SIT1 activity to balance plant growth and stress adaptation.

In this study, we used virus‐mediated gene silencing technology and found that the HSP17.4 gene‐silenced cultivar Sweet Charlie plants were more susceptible to Colletotrichum gloeosporioides than the wild‐type Sweet Charlie, and the level of infection was even higher than that of the susceptible cultivar Benihopp. The results of differential quantitative proteomics showed that after infection with the pathogen, the expression of the downstream response genes NPR1, TGA, and PR‐1 of the salicylic acid (SA) signalling pathway was fully up‐regulated in the wild‐type Sweet Charlie, and the expression of the core transcription factor MYC2 of the jasmonic acid (JA) pathway was significantly down‐regulated. The expression of the proteins encoded by these genes did not change significantly in the HSP17.4‐silenced Sweet Charlie, indicating that the expression of HSP17.4 activated the up‐regulation of downstream signals of SA and inhibited the JA signal pathway. The experiments that used SA, methyl jasmonate, and their inhibitors to treat plants provide additional evidence that the antagonism between SA and JA regulates the resistance of strawberry plants to C. gloeosporioides.