Partial substitution of chemical fertilizer by Trichoderma biofertilizer improved nitrogen use efficiency in wolfberry (Lycium chinense) in coastal saline land.

A two-year field trial was conducted to investigate the effects of partial substitution of chemical fertilizer (CF) by Trichoderma biofertilizer (TF) on nitrogen (N) use efficiency and associated mechanisms in wolfberry (Lycium chinense) in coastal saline land. As with plant biomass and fruit yield, apparent N use efficiency and plant N accumulation were also higher with TF plus 75% CF than 100% CF, indicating that TF substitution promoted plant growth and N uptake. As a reason, TF substitution stabilized soil N supply by mitigating steep deceases in soil NH4 +-N and NO3 -N concentrations in the second half of growing seasons. TF substitution also increased carbon (C) fixation according to higher photosynthetic rate (Pn) and stable 13C abundance with TF plus 75% CF than 100% CF. Importantly, leaf N accumulation significantly and positively related with Pn, biomass, and fruit yield, and structural equation modeling also confirmed the importance of the causal relation of N accumulation coupled with C fixation for biomass and yield formation. Consequently, physiological and agronomical N use efficiencies were significantly higher with TF plus 75% CF than 100% CF. Overall, partial substitution of CF by TF improved N use efficiency in wolfberry in coastal saline land by stabilizing soil N supply and coupling N accumulation with C fixation.

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To clarify the mechanisms underlying the improvement of Trichoderma on Chinese wolfberry (Lycium chinense) growth under saline stress, we analyzed the effects of application of organic fertilizer, Trichoderma agent and fertilizer on nitrogen uptake, assimilation, accumulation and use efficiency in Chinese wolfberry, based on a pot experiment with coastal saline soil. The organic fertilizer was the sterilization substance of Trichoderma fertilizer without viable Trichoderma, without any difference in the content of nutrients (such as nitrogen, phosphorus and potassium) between them. The results showed that the application of organic fertilizer, Trichoderma agent and ferti-lizer significantly increased NO3- and NH4+ influx rate in meristematic zone and NO3- influx rate in maturation zone of roots. The magnitude of such enhancement was greater in the application with Trichoderma fertilizer than organic fertilizer. Compared with the control, the application of Trichoderma agent and fertilizer significantly increased root, stem and leaf biomass and nitrogen content as well as plant nitrogen accumulation, strengthened root and leaf nitrate reductase, nitrite reductase and glutamine synthetase activities, and elevated nitrogen uptake efficiency, photosynthetic rate, stable carbon isotope abundance and photosynthetic nitrogen use efficiency. For all those variables, the beneficial effect was obviously stronger in the application with Trichoderma fertilizer than organic fertilizer. Therefore, Trichoderma facilitated nitrogen uptake, assimilation and accumulation in Chinese wolfberry under saline stress, improved photosynthetic carbon fixation ability and nitrogen use efficiency, and ultimately promoted plant growth.

Dissecting photosynthetic electron transport and photosystems performance in Jerusalem artichoke (Helianthus tuberosus L.) under salt stress.

Jerusalem artichoke (Helianthus tuberosus L.), a vegetable with medical applications, has a strong adaptability to marginal barren land, but the suitability as planting material in saline land remains to be evaluated. This study was envisaged to examine salt tolerance in Jerusalem artichoke from the angle of photosynthetic apparatus stability by dissecting the photosynthetic electron transport process. Potted plants were exposed to salt stress by watering with a nutrient solution supplemented with NaCl. Photosystem I (PSI) and photosystem II (PSII) photoinhibition appeared under salt stress, according to the significant decrease in the maximal photochemical efficiency of PSI (△MR/MR0) and PSII. Consistently, leaf hydrogen peroxide (H2O2) concentration and lipid peroxidation were remarkably elevated after 8 days of salt stress, confirming salt-induced oxidative stress. Besides photoinhibition of the PSII reaction center, the PSII donor side was also impaired under salt stress, as a K step emerged in the prompt chlorophyll transient, but the PSII acceptor side was more vulnerable, considering the decreased probability of an electron movement beyond the primary quinone (ETo/TRo) upon depressed upstream electron donation. The declined performance of entire PSII components inhibited electron inflow to PSI, but severe PSI photoinhibition was not averted. Notably, PSI photoinhibition elevated the excitation pressure of PSII (1-qP) by inhibiting the PSII acceptor side due to the negative and positive correlation of △MR/MR0 with 1-qP and ETo/TRo, respectively. Furthermore, excessive reduction of PSII acceptors side due to PSI photoinhibition was simulated by applying a specific inhibitor blocking electron transport beyond primary quinone, demonstrating that PSII photoinhibition was actually accelerated by PSI photoinhibition under salt stress. In conclusion, PSII and PSI vulnerabilities were proven in Jerusalem artichoke under salt stress, and PSII inactivation, which was a passive consequence of PSI photoinhibition, hardly helped protect PSI. As a salt-sensitive species, Jerusalem artichoke was recommended to be planted in non-saline marginal land or mild saline land with soil desalination measures.

ß-Conglycinin enhances autophagy in porcine enterocytes.

ß-Conglycinin (ß-CG) is well known for inducing intestinal allergies and dysfunction in neonates and young pigs. However, the underlying mechanisms are largely unknown. In this study, to clarify the role of autophagy in ß-CG-induced cytotoxicity, we investigated the effects of ß-CG on cell viability and autophagy activity in porcine enterocytes (IPEC-1 cells). The results indicated that the cell viability was decreased with the increasing levels of ß-CG. ß-CG treatment enhanced the eGFP-LC3 puncta per cells and LC3-II/LC3-I, and the latter was further increased in IPEC-1 cells cultured with bafilomycin A1. We conclude that ß-CG enhances autophagy activity in enterocytes.

N-acetylcysteine stimulates protein synthesis in enterocytes independently of glutathione synthesis.

Dietary supplementation with N-acetylcysteine (NAC) has been reported to improve intestinal health and treat gastrointestinal diseases. However, the underlying mechanisms are not fully understood. According to previous reports, NAC was thought to exert its effect through glutathione synthesis. This study tested the hypothesis that NAC enhances enterocyte growth and protein synthesis independently of cellular glutathione synthesis. Intestinal porcine epithelial cells were cultured for 3 days in Dulbecco's modified Eagle medium containing 0 or 100 µM NAC. To determine a possible role for GSH (the reduced form of glutathione) in mediating the effect of NAC on cell growth and protein synthesis, additional experiments were conducted using culture medium containing 100 µM GSH, 100 µM GSH ethyl ester (GSHee), diethylmaleate (a GSH-depletion agent; 10 µM), or a GSH-synthesis inhibitor (buthionine sulfoximine, BSO; 20 µM). NAC increased cell proliferation, GSH concentration, and protein synthesis, while inhibiting proteolysis. GSHee enhanced cell proliferation and GSH concentration without affecting protein synthesis but inhibited proteolysis. Conversely, BSO or diethylmaleate reduced cell proliferation and GSH concentration without affecting protein synthesis, while promoting protein degradation. At the signaling level, NAC augmented the protein abundance of total mTOR, phosphorylated mTOR, and phosphorylated 70S6 kinase as well as mRNA levels for mTOR and p70S6 kinase in IPEC-1 cells. Collectively, these results indicate that NAC upregulates expression of mTOR signaling proteins to stimulate protein synthesis in enterocytes independently of GSH generation. Our findings provide a hitherto unrecognized biochemical mechanism for beneficial effects of NAC in intestinal cells.