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- Author or Editor: Xiaohui Zhou x
Gummy stem blight (GSB) caused by the ascomycete fungus Didymella bryoniae (Auersw.) Rehm is an important disease of melon. Molecular markers linked to resistance would be useful for melon breeding programs. The amplified fragment length polymorphism (AFLP) technique and bulk segregant analysis were used to identify molecular markers linked to the resistance of melon to Didymella bryoniae. Segregation analysis of F2 progeny from a cross of PI 420145, a resistant line, and PI 136170, a susceptible line, showed that resistance to GSB was controlled by a dominant gene. One AFLP marker, E-TG/M-CTC200, was identified that is tightly linked to GSB resistance gene at a distance of 2.0 cM. To our best knowledge, this is the first report of AFLP markers linked to GSB resistance in melon. The identification of AFLP markers provides a step toward the use of marker-assisted selection and the characterization of the gene encoding resistance to GSB in melon.
Gummy stem blight incited by the fungus Didymella bryoniae is a major disease of melons worldwide. The objectives of the present study were to critically evaluate melon (Cucumis melo L.) germplasm for resistance to D. bryoniae and to characterize the genetics of resistance in the resistant accessions. Two hundred sources of germplasm (plant introduction accessions, cultivars, breeding lines, landraces, and wild relatives) were screened against a single highly virulent isolate (IS25) of D. bryoniae in a plastic tunnel. The genetics of resistance to D. bryoniae was studied in three crosses between plant introductions 157076, 420145, and 323498, resistant parents that were fairly adapted (flowering, fruiting, powdery mildew tolerance) to Nanjing conditions, and plant introductions 268227, 136170, and NSL 30032 susceptible parents, respectively. Six populations of each cross (susceptible parent, resistant parent, F1, F2, the two reciprocal backcrosses) were analyzed for their responses to D. bryoniae. Seedlings in both studies were inoculated with a spore suspension (5 × 105 spores/mL−1) of D. bryoniae at the four to six true-leaf stages and assessed for leaf and stem damage at 7, 14, and 21 d postinoculation. Results of germplasm screening indicated most germplasms reported as resistant elsewhere were confirmed resistant under our conditions. However, some plant introductions identified as highly resistant elsewhere were susceptible under our conditions, the most interesting being plant introduction 482399. This plant introduction that was considered resistant was highly susceptible in our study. We also identified other sources of resistance not reported previously, for example, JF1; a wild Cucumis from the highlands of Kenya was rated highly resistant. Analysis of segregation of F1, F2, and backcross generations of the three crosses indicated that each of the three plant introductions carry a single dominant gene for resistance to the D. bryoniae.
We studied the effects of exogenous spermidine (Spd) on plant growth and nitrogen metabolism in two cultivars of tomato (Solanum lycopersicum) that have differential sensitivity to mixed salinity-alkalinity stress: ‘Jinpeng Chaoguan’ (salt-tolerant) and ‘Zhongza No. 9’ (salt-sensitive). Seedling growth of both tomato cultivars was inhibited by salinity-alkalinity stress, but Spd treatment alleviated the growth reduction to some extent, especially in ‘Zhongza No. 9’. Exogenous Spd may help reduce stress-induced increases in free amino acids, ammonium (NH4 +) contents, and NADH-dependent glutamate dehydrogenase (NADH-GDH) activities; depress stress-induced decreases in soluble protein and nitrate content; and depress nitrate reductase, nitrite reductase, glutamine synthetase (GS), NADH-dependent glutamate synthase (NADH-GOGAT), glutamate oxaloacetate transaminase (GOT), and glutamate pyruvate transaminase (GPT) activities, especially for ‘Zhongza No. 9’. Based on our results, we suggest that exogenous Spd promotes the assimilation of excess toxic NH4 + by coordinating and strengthening the synergistic action of NADH-GDH, GS/NADH-GOGAT, and transamination pathways, all during saline-alkaline stress. Subsequently, NH4 + and its related enzymes (GDH, GS, GOGAT, GOT, and GPT), in vivo, are maintained in a proper and balanced state to enable mitigation of stress-resulted damages. These results suggest that exogenous Spd treatment can relieve nitrogen metabolic disturbances caused by salinity-alkalinity stress and eventually promote plant growth.