Improving rice nitrogen-use efficiency by modulating a novel monouniquitination machinery for optimal root plasticity response to nitrogen.

Plant nitrogen (N)-use efficiency (NUE) is largely determined by the ability of root to take up external N sources, whose availability and distribution in turn trigger the modification of root system architecture (RSA) for N foraging. Therefore, improving N-responsive reshaping of RSA for optimal N absorption is a major target for developing crops with high NUE. In this study, we identified RNR10 (REGULATOR OF N-RESPONSIVE RSA ON CHROMOSOME 10) as the causal gene that underlies the significantly different root developmental plasticity in response to changes in N level exhibited by the indica (Xian) and japonica (Geng) subspecies of rice. RNR10 encodes an F-box protein that interacts with a negative regulator of auxin biosynthesis, DNR1 (DULL NITROGEN RESPONSE1). Interestingly, RNR10 monoubiquitinates DNR1 and inhibits its degradation, thus antagonizing auxin accumulation, which results in reduced root responsivity to N and nitrate (NO3-) uptake. Therefore, modulating the RNR10-DNR1-auxin module provides a novel strategy for coordinating a desirable RSA and enhanced N acquisition for future sustainable agriculture.

Zeolite/ZnAl-layer double hydroxides with different Zn/Al ratios and intercalated anions as the substrate of constructed wetlands: synthesis, characterization and purification effect of Hexavalent chromium.

The study aimed to synthesize novel zeolite substrates modified with four types of ZnAl-LDHs including Cl-LDHs(1:1), Cl-LDHs(3:1), CO3-LDHs(1:1), and CO3-LDHs(3:1); investigate Cr(VI) removal efficiencies in lab-scale constructed wetlands (CWs); and explore the effect of different Zn/Al ratios and intercalated anions on the removal efficiencies of Cr(VI) by modified zeolite. Different ZnAl-LDHs were prepared by co-precipitation method and coated onto the surface of original zeolite. Field emission scanning electron microscope and energy dispersive spectrometer were used to analyze physicochemical properties of zeolite/ZnAl-LDHs. Obtained results confirmed the successful LDHs-coating modification. The results of both X-ray diffraction and Fourier transform infrared suggested that the typical diffraction peak and functional groups of ZnAl-LDHs were detected in modified zeolites, and the peak of CO32- in CO3-LDHs at 1362 cm-1 was stronger and sharper than Cl-LDHs. It could be demonstrated by above results that the synthesis crystallinity and coating effect of CO3-LDHs was better than Cl-LDHs. Furthermore, it could be found that under the condition of same intercalated anion, LDHs with metal molar ratio of 1:1 had better crystallinity than LDHs with metal molar ratio of 3: 1. Subsequent determination of the removal performance of Cr(VI) by purification experiments revealed that zeolite/Cl-LDHs(3:1) showed the best Cr(VI) removal performance, and the removal rate of Cr(VI) was improved by 32.81% compared with the original zeolite, which suggested that could be an efficient substrate of CWs for Cr(VI) removal. The high crystallinity indicated that the structure of LDHs was stable and it was difficult to remove Cr(VI) by ion exchange. The above explained why the Cr(VI) removal efficiency by zeolite/Cl-LDHs is superior to that by zeolite/CO3-LDHs under the condition of same metal molar ratio. With the increase of metal molar ratio, the charge density of LDHs layers and intercalated anion increased, thus enhancing the electrostatic attraction of LDHs layers to Cr(VI) and the interlayer anion exchange capacity. However, the effect of charge density on Cr(VI) removal efficiency may be greater than crystallinity on removal efficiency, which could be responsible for the fact that zeolite/ZnAl-LDHs(3:1) had better Cr(VI) removal efficiency than zeolite/ZnAl-LDHs(1:1) under the condition of same intercalated anion.

Centrally administered apelin-13 induces depression-like behavior in mice.

Apelin, a novel bioactive peptide highly concentrated in the brain, is identified as the endogenous ligand for angiotensin-like 1 receptor (APJ). The present study was designed to investigate the effect of apelin-13 on emotion-related behavior using the forced swimming test (FST) and tail suspension test (TST). Intracerebroventricular (i.c.v.) administration of apelin-13 (0.3, 1 and 3µg/mouse) dose-dependently increased the immobility time in the FST and TST, compared with control group. However, the APJ receptor antagonist apelin-13(F13A) (0.3-10µg/mouse, i.c.v.) had no influence on immobility time in the FST. The increase of immobility time induced by apelin-13 was significantly blocked by apelin-13(F13A), non-selective opioid receptor antagonist naloxone and κ-opioid receptor antagonist nor-binaltorphimine dihydrochloride (nor-BNI), respectively, but not the non-selective corticotrophin-releasing factor (CRF) receptor antagonist α-helical CRF(9-41) in the FST. In order to eliminate the possibility of a false-positive result in the FST or TST, spontaneous activity and motor function were checked. The results demonstrate that apelin-13 alone or antagonists co-administered with apelin-13 did influence spontaneous activity counts. And apelin-13 had no effect on the motor behavior in the rotarod test and wire hanging test. These results indicate that centrally administered apelin-13 elicited depression-like behavior in mice, which was mediated via APJ receptor and κ-opioid receptor, but not CRF receptor.

Supraspinal antinociceptive effect of apelin-13 in a mouse visceral pain model.

Apelin, as the endogenous ligand of the APJ receptor, is a novel identified neuropeptide whose biological functions are not fully understood. APJ receptor mRNA was found in several brain regions related to descending control system of pain, such as amygdala, hypothalamus and dorsal raphe nucleus (DRN). The present study was designed to determine whether supraspinal apelin-13 may produce antinociceptive effect observed in the acetic acid-induced writhing test, a model of visceral pain. Apelin-13 not only significantly produced preemptive antinociception at the dose of 0.3, 0.5, 1 and 3 µg/mouse when injected intracerebroventricularly (i.c.v.) before acetic acid, but also significantly induced antinociception at a dose of 0.5, 1 and 3 µg/mouse when injected i.c.v. after acetic acid. And i.c.v. apelin-13 did not influence 30-min locomotor activity counts in mice. Intrathecal (i.t.) administration of apelin-13 (1 and 3 µg/mouse) significantly decreased the number of writhes, however, intraperitoneal (i.p.) injection of apelin-13 (10-100 µg/mouse) had no effect on the number of writhes in the writhing test. The specific APJ receptor antagonist apelin-13(F13A), no-specific opioid receptor antagonist naloxone and µ-opioid receptor antagonist ß-funaltrexamine hydrochloride (ß-FNA) could significantly antagonize the antinociceptive effect of i.c.v. apelin-13, suggesting APJ receptor and µ-opioid receptor are involved in this process. Central low dose of apelin-13 (0.3 µg/mouse, i.c.v.) could significantly potentiate the analgesic potencies of modest and even relatively ineffective doses of morphine administrated at supraspinal level. This enhanced antinociceptive effect was reversed by naloxone, suggesting that the potentiated analgesic response is mediated by opioid-responsive neurons.

Central apelin-13 inhibits food intake via the CRF receptor in mice.

Apelin, the novel identified peptide, is the endogenous ligand for the APJ. Previous studies have reported the effect of apelin on food intake, however the action of acute central injected apelin on food intake in mice remains unknown. The present study was designed to investigate the mechanism as well as the effect of central apelin-13 on food intake in mice. During the dark period, the cumulative food intake was significantly decreased at 4h after the intracerebroventricular (i.c.v.) injection of 1 and 3µg/mouse apelin-13 and the period food intake was significantly reduced during 2-4h after treatment. In the fasted mice, the cumulative food intake was significantly decreased at 2 and 4h after injection of 3µg/mouse apelin-13. The cumulative water intake was significantly reduced by apelin-13 (3µg/mouse) at 4h after injection in freely feeding and fasted mice. However, during light period, apelin-13 had no influence on food and water intake in freely feeding mice. The APJ receptor antagonist apelin-13(F13A) (6µg/mouse) and the corticotrophin-releasing factor (CRF) receptor antagonist α-helical CRF(9-41) (3µg/mouse) could reverse the inhibitory effect on cumulative food intake/0-4h induced by apelin-13 (3µg/mouse) in freely feeding mice during the dark period, whereas the anorexic effect could not be antagonized by the arginie vasopressin (AVP) receptor antagonist deamino(CH(2))(5)Tyr(Me)AVP (0.5µg/mouse). Taken together, these results suggest that central apelin-13 inhibits food intake in mice and it seems that APJ receptor and CRF receptor, but not AVP receptor, might be involved in this process.

Effect of centrally administered apelin-13 on gastric emptying and gastrointestinal transit in mice.

Apelin, as the endogenous ligand for the APJ, regulates many biological functions, including blood pressure, neuroendocrine, drinking behavior, food intake and colonic motility. The present study was designed to investigate the effect of central apelin-13 on gastric emptying and gastrointestinal transit in mice. Intracerebroventricular (i.c.v.) injection of apelin-13 (3 and 10 µg/mouse) decreased gastric emptying rate by 10.9% and 17.1%. This effect was significantly antagonized by the APJ receptor antagonist apelin-13(F13A) and the opioid receptor antagonist naloxone, respectively. However, intraperitoneal (i.p.) injection of apelin-13 (10-100 µg/mouse) did not affect gastric emptying. Apelin-13 (0.3, 1 and 3 µg/mouse, i.c.v.) inhibited gastrointestinal transit by 16.8%, 23.4% and 19.2%. Apelin-13(F13A) and naloxone could also reverse this antitransit effect induced by apelin-13. Taken together, these results suggest that i.c.v. injected apelin-13 inhibits gastric emptying and gastrointestinal transit and it seems that APJ receptor and opioid receptor might be involved in these processes.