Knockout of SlDCL2b attenuates the resistance of tomato to potato spindle tuber viroid infection.

RNA interference, or RNA silencing, is an important defence mechanism against viroid infection in plants. Plants encode multiple DICER-LIKE (DCL) proteins that are key components of the RNA silencing pathway. However, the roles of different DCLs in defence responses against viroid infection remain unclear. Here, we determined the function of tomato DCL2b (SlDCL2b) in defence responses against potato spindle tuber viroid (PSTVd) infection using SlDCL2b loss-of-function tomato mutant plants. Compared with wild-type plants, mutant plants were more susceptible to PSTVd infection, developing more severe symptoms earlier and accumulating higher levels of PSTVd RNAs. Moreover, we verified the feedback mechanism for the regulation of SlDCL2b expression by miR6026. Functional blocking of tomato miR6026, by expressing its target mimics, can enhance resistance to PSTVd infection in tomato plants. These findings deepen the current understanding of RNAi-based resistance against viroid infection and provide a potentially new strategy for viroid control.

Shift in the Mode of Carbon Cycling Recorded by Biomarkers and Carbon Isotopic Compositions in the Yanchang Formation, Ordos Basin: Autotrophy vs Heterotrophy.

Organic-rich shales and mudstones have long been investigated regarding the control of source, environment, climate, etc. on the enrichment of organic carbon. However, little is documented about how autotrophy and heterotrophy influence organic carbon cycling/export. Here, we show molecular and carbon isotopic compositional changes of the shale or mudstone source rocks from the Chang 3 to 7 members of the Yanchang Formation. The Chang 7 member source rocks have higher quality (480-500 mg/g) and total organic carbon (TOC) (15.3% on average) than other member source rocks; the sterane/hopane ratio and the δ13C of organic carbon and kerogen decrease from the Chang 3 to 7 members, but Δδ ([average δ13C of n-C17 + n-C18] - [average δ13C of pristane + phytane]) increases, and no aryl isoprenoids and C40 aromatic carotenoids (e.g., isorenieratane) were observed. These low maturity biomarker features suggest that there were no water stratification, photic zone euxinia (PZE), and no obvious change in the organic matter source, and the water column is generally anoxic. A comparison of the δ13C of Pr and Ph with the δ13C of the n-C17 and n-C18 alkanes reveals a shift in the mode of carbon cycling/export (autotrophy versus heterotrophy) in the Yanchang Formation and that there was dominant heterotrophic bacterial activity or bacterial biomass in the Chang 7 member. The TOC spike in the Chang 7 member may result from boosted carbon cycling/export that improves organic carbon preservation than other members. Possible external forcings on the shift are abundant hydrothermal- or volcanic-derived metal salts as electron acceptors in the palaeowater, which is a reasonable explanation for enhanced heterotrophic bacterial activity. This finding improves our understanding of heterotrophic bacterial activity control on organic matter (OM) preservation and may be a significant supplement for understanding the ecological or environmental forcings in the Yanchang Formation, Ordos Basin.

Effects of sodium butyrate supplementation on inflammation, gut microbiota, and short-chain fatty acids in Helicobacter pylori-infected mice.

BACKGROUND: Inflammation induced by Helicobacter pylori (H. pylori) infection is the basis for the pathogenesis of H. pylori. Butyric acid, a diet-related microbial-associated metabolite, is connected to inflammation, metabolic syndrome, and other diseases. Several studies have indicated the effects of sodium butyrate (SB) against bacteria; however, the effects of SB on the main virulence factors of H. pylori, H. pylori-induced inflammation, and gut microbiota composition remain unclear. MATERIALS AND METHODS: SB was supplemented in H. pylori coculture and administered to mice infected with H. pylori. The effects of SB intake on inflammation, gut microbiota composition, and short-chain fatty acids (SCFAs) in H. pylori-infected mice were assessed. RESULTS: The in vitro experiments demonstrated that SB not only inhibited the growth of H. pylori but also decreased the mRNA expression of CagA and VacA. SB intake reduced the production of virulence factors in H. pylori-infected mice, inhibited the IκBα/NF-κB pathway by reducing the expression of Toll-like receptors (TLRs), and reduced the production of TNF-α and IL-8. Further analysis demonstrated that H. pylori infection altered the relative abundance of the intestinal microbial community in mice. The level of SCFAs in the feces of H. pylori-infected mice was changed, although the intake of SB did not obviously change the level of SCFAs. CONCLUSIONS: Our study showed that SB may decrease H. pylori-induced inflammation by inhibiting the viability and virulence of H. pylori and may reduce inflammation in association with the gut microbiota in H. pylori-infected mice. This study may provide novel insights into the mechanisms by which SB, a diet-related microbial-associated metabolite, affects H. pylori-induced disease development.

[Study on the mechanism of naofucong granule in improving memory of cerebral ischemic mice].

OBJECTIVE: To explore the effect of Naofucong Granule (NFCG), a self-manufactured Chinese herbal preparation, on memory and cerebral cholinergic system in cerebral ischemic mice. METHODS: Mice model of learning/memory impairment was established by bilateral ligation of internal carotid arteries. The memory ability of mice was assessed by measuring latent period in the Morris Water Maze. RESULTS: Seven days after modeling, the latent period and swimming course of mice (82.3 +/- 32.0 seconds and 986.7 +/- 414.5 cm) were longer than those of control (sham-operated mice, 35.3 +/- 37.9 seconds and 410.4 +/- 507.0 cm, P < 0.01). Administration of NFCG could ameliorate these changes to 30.6 +/- 31.3 seconds and 378.1 +/- 386.3 cm (P < 0.01) and normalized. In the model animals, the choline acetylase activity in brain cortex and hippocampus was 35.64 +/- 4.96 and 45.08 +/- 4.96 respectively, which was significantly lower than that in the control (40.52 +/- 4.74 and 53.96 +/- 8.53); so was the activity of cholinergic receptor M in cerebral cortex (44.41 +/- 10.67 vs 57.56 +/- 6.98) and the activity of cholinergic receptor N in cerebral cortex and hippocampus (232.41 +/- 21.99 and 303.72 +/- 72 +/- 28.78 vs 276.66 +/- 32.46 and 385.56 +/- 46.88), P < 0.05 or P < 0.01. Administration of NFCG also could reverse them and elevate to normal level. CONCLUSION: NFCG has protective function on intellectual deficits in cerebral ischemic mice, which may be related to its action in enhancing function of cholinergic system.