Small auxin up RNA (SAUR) is a large gene family that is widely distributed among land plants. In this study, a comprehensive analysis of the SAUR family was performed in sweet cherry, and the potential biological functions of PavSAUR55 were identified using the method of genetic transformation. The sweet cherry genome encodes 86 SAUR members, the majority of which are intron-less. These genes appear to be divided into seven subfamilies through evolution. Gene duplication events indicate that fragment duplication and tandem duplication events occurred in the sweet cherry. Most of the members mainly underwent purification selection pressure during evolution. During fruit development, the expression levels of PavSAUR16/45/56/63 were up-regulated, and conversely, those of PavSAUR12/61 were down-regulated. Due to the significantly differential expressions of PavSAUR13/16/55/61 during the fruitlet abscission process, they might be the candidate genes involved in the regulation of physiological fruit abscission in sweet cherry. Overexpression of PavSAUR55 in Arabidopsis produced earlier reproductive growth, root elongation, and delayed petal abscission. In addition, this gene did not cause any change in the germination time of seeds and was able to increase the number of lateral roots under abscisic acid (ABA) treatment. The identified SAURs of sweet cherry play a crucial role in fruitlet abscission and will facilitate future insights into the mechanism underlying the heavy fruitlet abscission that can occur in this fruit crop.
Pear anthracnose, caused by Colletotrichum fructicola, is a devastating disease that seriously affects most pear varieties, thereby compromising their yield and quality. However, effective control of this pathogen is lacking. Moreover, the critical resistance responses to C. fructicola in pear are unknown. To investigate these resistance mechanisms of pear against Colletotrichum fructicola, transcriptomic and metabolomic were performed and analyzed in pear anthracnose-resistant pear variety ‘Seli’ and the susceptible variety ‘Cuiguan’ after infection with C. fructicola, respectively. The differentially expressed genes and differentially accumulated metabolites (DAMs) were mainly related to metabolism and secondary metabolite synthetic pathways, including alpha-linoleic acid metabolism, phenylalanine biosynthesis metabolism, unsaturated fatty acids biosynthesis, and amino acids and derivatives biosynthesis etc. In particular, the accumulation of unsaturated fatty acids, amino acids and derivatives, such as linoleic acid and derivatives, lauric acid, N-acetyl-L-glutamic acid and L-proline was significantly increased in the resistant pear variety ‘Seli’ upon C. fructicola infection, while the amino acids of oxiglutatione and N-acetyl-L-glutamic acid, as well as the proanthocyanidins were significantly decreased in susceptible pear variety ‘Cuiguan’ upon C. fructicola infection, indicating that these metabolites were responsible for the different levels of resistance to anthracnose in ‘Seli’ and ‘Cuiguan’. Overall, our results provided new insights into pear anthracnose resistance regulation, and this may assist in developing new strategies to control pear anthracnose, as well as in breeding anthracnose-resistant varieties.
Tartary buckwheat (Fagopyrum tataricum), an under-utilized pseudocereal, has important nutritional and pharmaceutical properties and is resistant to drought and nutrient deficiency. However, this environmentally friendly crop is sensitive to salt stress that can result in water loss, stomatal closure, affect photosynthesis and metabolism, and reduce yield and quality of Tartary buckwheat. Thus, it is important to understand the mechanism of salt stress tolerance in buckwheat. In this study, we identified a locus including 35 candidate genes on chromosome 2 that is significantly associated with salt tolerance of Tartary buckwheat by genome-wide association analysis (GWAS). Transcriptome analysis revealed that the serine/threonine-protein kinase Aurora-3 (FtAUR3) family gene was up-regulated in response to salt stress. The deletion of a single nucleotide in the FtAUR3 promoter leads to increased FtAUR3 expression and enhanced salt tolerance in Tartary buckwheat. Overexpression of FtAUR3 in buckwheat hairy roots leads to the accumulation of flavonoids, including rutin and cinnamic acid, as well as the induction of the expression of flavonoid biosynthesis genes, such as PAL, C4H, F3H and F3’H, under salt stress. In addition, it was shown that over-expression of FtAUR3 in Arabidopsis thaliana induced the expression of salt-resistant genes (SOS1, AVP1, etc.) and enhanced salt tolerance compared to wild type plants. Furthermore, under salt stress, FtAUR3 can significantly enhances the levels of reactive oxygen species pathway components, including superoxide dismutase, catalase, and peroxidase, thereby improving plant salt tolerance. Thus, we demonstrated that FtAUR3 interacts with the critical enzyme FtGAPB in the ROS pathway, suggesting a potential mechanism through which FtAUR3 contributes to ROS signaling. Taken together, these results demonstrated that FtAUR3 may play a critical positive role in Tartary buckwheat resistance against salt stress.