How abiotic stresses trigger sugar signaling to modulate leaf senescence?

Plants have evolved the adaptive capacity to mitigate the negative effect of external adversities at chemical, molecular, cellular, and physiological levels. This capacity is conferred by triggering the coordinated action of internal regulatory factors, in which sugars play an essential role in the regulating chloroplast degradation and leaf senescence under various stresses. In this review, we summarize the recent findings on the senescent-associated changes in carbohydrate metabolism and its relation to chlorophyl degradation, oxidative damage, photosynthesis inhibition, programmed cell death (PCD), and sink-source relation as affected by abiotic stresses. The action of sugar signaling in regulating the initiation and progression of leaf senescence under abiotic stresses involves interactions with various plant hormones, reactive oxygen species (ROS) burst, and protein kinases. This discussion aims to elucidate the complex regulatory network and molecular mechanisms that underline sugar-induced leaf senescence in response to various abiotic stresses. The imperative role of sugar signaling in regulating plant stress responses potentially enables the production of crop plants with modified sugar metabolism. This, in turn, may facilitate the engineering of plants with improved stress responses, optimal life span and higher yield achievement.

Rice ins(3)P synthase1 (RINO1) participates in embryonic development by regulating inositol-associated changes in auxin synthesis and its distribution.

The breeding of low phytic acid (LPA) crops is widely considered an effective strategy to improve crop nutrition, but the LPA crops usually have inferior seed germination performance. To clarify the reason for the suboptimal seed performance of LPA rice, this study investigated the impact of reduced seed phytic acid (InsP6) content in rice ins(3)P synthase1 (EC 5.5.1.4, RINO1), one of the key targets for engineering LPA rice, knockouton cellular differentiation in seed embryos and its relation to myo-inositol metabolism and auxin signalling during embryogenesis. The results indicated that the homozygotes of RINO1 knockout could initiate differentiation at the early stage of embryogenesis but failed to form normal differentiation of plumule and radicle primordia. The loss of RINO1 function disrupted vesicle trafficking and auxin signalling due to the significantly lowered phosphatidylinositides (PIs) concentration in seed embryos, thereby leading to the defects of seed embryos without the recognizable differentiation of shoot apex meristem (SAM) and radicle apex meristem (RAM) for the homozygotes of RINO1 knockout. The abnormal embryo phenotype of RINO1 homozygotes was partially rescued by exogenous spraying of inositol and indole-3-acetic acid (IAA) in rice panicle. Thus, RINO1 is crucial for both seed InsP6 biosynthesis and embryonic development. The lower phosphatidylinositol (4,5)-bisphosphate (PI (4,5) P2) concentration and the disorder auxin distribution induced by insufficient inositol supply in seed embryos were among the regulatory switch steps leading to aberrant embryogenesis and failure of seed germination in RINO1 knockout.

Involvement of plant signaling network and cell metabolic homeostasis in nitrogen deficiency-induced early leaf senescence.

Nitrogen (N) is a basic building block that plays an essential role in the maintenance of normal plant growth and its metabolic functions through complex regulatory networks. Such the N metabolic network comprises a series of transcription factors (TFs), with the coordinated actions of phytohormone and sugar signaling to sustain cell homeostasis. The fluctuating N concentration in plant tissues alters the sensitivity of several signaling pathways to stressful environments and regulates the senescent-associated changes in cellular structure and metabolic process. Here, we review recent advances in the interaction between N assimilation and carbon metabolism in response to N deficiency and its regulation to the nutrient remobilization from source to sink during leaf senescence. The regulatory networks of N and sugar signaling for N deficiency-induced leaf senescence is further discussed to explain the effects of N deficiency on chloroplast disassembly, reactive oxygen species (ROS) burst, asparagine metabolism, sugar transport, autophagy process, Ca2+ signaling, circadian clock response, brassinazole-resistant 1 (BZRI), and other stress cell signaling. A comprehensive understanding for the metabolic mechanism and regulatory network underlying N deficiency-induced leaf senescence may provide a theoretical guide to optimize the source-sink relationship during grain filling for the achievement of high yield by a selection of crop cultivars with the properly prolonged lifespan of functional leaves and/or by appropriate agronomic managements.

Disruptions of sugar utilization and carbohydrate metabolism in rice developing anthers aggravated heat stress-induced pollen abortion.

High temperature (HT) stress at reproductive stage is one of most important environment negatively affecting spikelet fertility and rice yield. In this study, the effect of HT exposure on the sugar composition and carbohydrate metabolism in developing anthers and its relation to floret fertility and pollen viability were investigated by different temperature regimes under well-controlled climatic condition. Result showed that HT exposure during microspore development significantly reduced the starch deposition in developing anther and evidently disrupted the spatial distribution of sugar and starch concentrations in different compartments of rice anther, with the higher ratio of sucrose to hexose concentrations in HT-stressed anthers relative to the control ones. Under HT exposure, the amount of starch deposition in the fraction of sporophytic tissues dropped evidently, while the concentrations of sucrose and starch in anther wall tissue enhanced significantly, suggesting that HT exposure impaired the translocation of sucrose from the anther wall tissue to the sporophytic tissues inside rice anther. Furthermore, we presented possible contribution of various genes and key enzymes involving in sugar conversion and carbohydrate metabolism in developing anther to the formation of HT-induced pollen abortion by disrupting the sugar utilization in HT-stressed anther. HT exposure suppressed the activities of cell wall and vacuolar invertase, hexokinase, and ADP-glucose pyrophosphorylase in developing anther, while it was opposite for the effect of HT exposure on sucrose synthase and fructokinase. HT-induced suppression of OsCWIN3 in the anther walls might be strongly responsible for the HT-induced impairments of sugar utilization in HT-stressed anthers.

ABA-triggered ROS burst in rice developing anthers is critical for tapetal programmed cell death induction and heat stress-induced pollen abortion.

High temperatures (HT) cause pollen abortion and poor floret fertility in rice, which is closely associated with excessive accumulation of reactive oxygen species (ROS) in the developing anthers. However, the relationships between accumulation of abscisic acid (ABA) and ROS, and their effects on tapetum-specific programmed cell death (PCD) in HT-stressed anthers are poorly characterised. Here, we determined the spatiotemporal changes in ABA and ROS levels, and their relationships with tapetal PCD under HT exposure. Mutants lacking ABA-activated protein kinase 2 (SAPK2) functions and exogenous ABA treatments were used to explore the effects of ABA signalling on the induction of PCD and ROS accumulation during pollen development. HT-induced pollen abortion was tightly associated with ABA accumulation and oxidative stress. The higher ABA level in HT-stressed anthers resulted in the earlier initiation of PCD induction and subsequently abnormal tapetum degeneration by activating ROS accumulation in developing anthers. Interactions between SAPK2 and DEAD-box ATP-dependent RNA helicase elF4A-1 (RH4) were required for ABA-induced ROS generation in developing anthers. The OsSAPK2 knockout mutants showed the impaired PCD responses in the absence of HT. However, the deficiency of SAPK2 functions did not suppress the ABA-mediated ROS generation in HT-stressed anthers.

SLAMF8 promotes the proliferation and migration of synovial fibroblasts by regulating the ERK/MMPs signalling pathway.

Rheumatoid arthritis is troublesome to treat effectively and often requires concomitant long-term treatment. Meanwhile, synovial fibroblasts could induce inflammation response and lead to joint erosion, finally causing progressive joint destruction, disability, and increased mortality. This study focussed on the role of SLAM family member 8 (SLAMF8) in mediating cell function from rheumatoid arthritis synovial fibroblasts stimulated with TNF-α. Cell Counting Kit-8 (CCK-8) and colony-forming unit assay were used to evaluate cell proliferation. SLAMF8 expression was analysed by reverse transcription-quantitative PCR (RT-qPCR) and western blot. Annexin V-FITC/PI double staining was used to measure the apoptosis rate. The cell migration and invasion in TNF-α-stimulated MH7A (human rheumatoid arthritis synovial cell line) and HFLS-RA cells (human fibroblast-like synoviocytes: rheumatoid arthritis) were tested via wound healing assay and transwell migration assay. In the present study, after TNF-α treatments, the SLAMF8 mRNA and protein expression in both MH7A and HFLS-RA cell lines have a time-dependent increase. The attenuation of SLAMF8 ameliorated TNF-α-induced proliferation, invasion and migration in MH7A and HFLS-RA cells. Simultaneously, when SLAMF8 was silenced, the expression of p-ERK, MMP-1, and MMP-13 was suppressed significantly. In summary, these results indicated that the knockdown of the SLAMF8 significantly attenuated TNF-α-induced proinflammatory responses in MH7A and HFLS-RA cells. Therefore, SLAMF8 exhibits therapeutic potential for the management of inflammation in rheumatoid arthritis.

Combined Effect of Nitrogen Fertilizer Application and High Temperature on Grain Quality Properties of Cooked Rice.

Ambient temperature and nitrogen (N) fertilizer are two of the most important factors that affect rice grain quality. However, less information has been available on the interactive effect of N fertilizer and ambient temperature on grain quality under stressful high temperature (HT). In this article, the effects of panicle N fertilizer, ambient temperature, and their interaction on starch composition, particle size distribution of starch granules, starch physicochemical properties, and storage protein accumulation in milled grains were investigated to clarify the potential role of panicle N fertilizer topdressing in regulating rice grain quality under stressful HT by using a two-factor experiment of three N levels in combination with two temperature regimes. Results showed that appropriate application of panicle N fertilizer could attenuate the adverse effect of HT during grain filling on milling quality and chalky occurrence to some extent, particularly for the effective alleviation of HT-induced decrease in milling quality. However, the topdressing of panicle N fertilizer tended to enhance starch gelatinization enthalpy (ΔH) and its setback viscosity in HT-ripening grains, with the simultaneous decrements in the number and surface area proportions of smaller starch granules under the higher N fertilizer in combination with HT exposure. The effects of higher nitrogen fertilizer and HT exposure on total protein content and gluten composition of grains were additively increased. Hence, the topdressing of panicle N fertilizer exacerbated HT-induced deterioration in cooking and eating quality, rather than alleviating the negative impact of HT exposure on the palatability of cooked rice.

Effect of Glucocorticoid Nanoliposomes on Vascular Endothelial Growth Factor Expression in Brain Tissue of Rats with Tuberculous Meningitis.

To investigate the effect of human brain-targeted nanoliposomes encapsulating methylprednisolone sodium succinate on the level of vascular endothelial growth factor (VEGF) in brain tissue of rats with tuberculous meningitis (TBM), the nanoliposome DSPE-125I-AIBZM-MPS was prepared. 180 rats were divided into normal control, TBM infection, and TBM treatment groups. The brain water content, Evans blue (EB) content, VEGF, and the gene and protein expression of receptors (Flt-1, Flk-1) of rats after modeling were measured. The brain water content and EB content in the TBM treatment group were significantly lower than those in the TBM infection group at 4 and 7 days after modeling (P < 0.05). The expression of VEGF and its receptor Flt-1 mRNA in the brain tissue of rats in the TBM infection group was significantly higher than that in the normal control group at 1, 4, and 7 days after modeling (P < 0.05). The expression of VEGF and its receptor Flt-1 mRNA in the brain tissue of rats in the TBM treatment group was significantly higher than that in the TBM infection group at 1, 4, and 7 days after modeling (P < 0.05). In summary, the prepared DSPE-125I-AIBZM-MPS nanoliposomes can effectively reduce brain water content and EB content and reduce the release of inflammatory factors of brain tissue in rats, playing a role in the treatment of TBM in rats by regulating the expression of VEGF and its receptor Flt-1 mRNA.

Targeted Therapy of Tuberculous Meningitis in Rats with Methylprednisolone Composite Nanoparticles.

It was to investigate the targeted therapeutic effect of methylprednisolone (MPS) composite nanoparticles (NPs) on tuberculous meningitis (TBM) in rats. A total of 180 special pathogen-free (SPF) Sprague Dawley (SD) rats (male) were randomly and equally assigned to the normal control group, TBM infection group, and TBM treatment group. Those in the TBM infection group and the TBM treatment group were injected with Mycobacterium tuberculosis suspension via the tail vein. After the TBM model was established, rats in the TBM treatment group were injected intraperitoneally with methylprednisolone-nano sterically stabilized liposomes (MPS-NSSLs), and those in the normal control group were injected with an equal amount of normal saline. MPS-NSSLs were prepared, and their quality evaluation, encapsulation rate, drug-lipid ratio, and stability were detected. The particle size distribution of MPS-NSSLs was 95.4 ± 0.7 nm, showing a complete spherical structure, and the encapsulation rate was 91.24 ± 0.27 %, and the drug-lipid ratio was about 0.4. After 7 days of treatment, the water content of brain tissue in the TBM infection group was drastically superior to that in the control group (P<0.05); Evans blue (EB) content in the TBM infection group was dramatically superior to that in the control group (P<0.05). The TBM rat model was successfully established, and this model verified that MPS-NSSLs had the characteristics of high efficiency and low toxicity in the treatment of TBM rats.

SSIIIa-RNAi suppression associated changes in rice grain quality and starch biosynthesis metabolism in response to high temperature.

High temperature (HT) is a main environmental restraint that affects rice yield and grain quality. In this study, SSIIIa-RNAi and its wild-type (WT) were used to investigate the effect of HT exposure on the isozyme-specific variation of several key starch biosynthesis enzymes in developing endosperms and its relation to starch properties. SSIIIa-RNAi had minimal impact on grain chalky occurrence under normal temperature growth, but it could up-grade the susceptibility of grain chalky occurrence to HT exposure, due to the relatively sensitive response of AGPase and SSI to HT exposure. Different from WT, SSIIIa-RNAi had the relatively enriched proportion of chains with DP 13-16 under HT, and HT-induced decline in the proportion of DP < 12 became much larger for SSIIIa-RNAi relative to WT. SSIIIa-RNAi significantly enhanced the expression of SSI isozyme and total SS activity, whereas SSI-RNAi deficiency had little impact on the expression of SSIIIa isozyme. In this regard, the compensatory increase in SSI isozyme as a result of SSIIIa deficiency occurred only in a one-way manner. SSIIIa-RNAi caused a striking elevation in BEIIa expression, and the effect of SSIIIa deficiency on the chain length distribution in relation to HT exposure was closely associated with the participation of BEIIa, SSI, and their interaction in amylopectin biosynthesis.

The effects of selenium on polyunsaturated fatty acids of Diasporangium jonesianum.

Fungi had become the main resource of polyunsaturated fatty acids, especially linoleic acid. The research studied the effects and mechanism of selenium on polyunsaturated fatty acids of Diasporangium jonesianum. The results showed that selenium could significantly increase the yields of linoleic acid. In contrast, the growth and γ-linolenic acid yield of D. jonesianum was decreased under selenium treatments. Δ6-Fatty acid desaturase gene of D. jonesianum was investigated in this research. Sequence analysis indicated that this cDNA sequence encoded 235 amino acids. The conserved region of Δ6-fatty acid desaturase included three conserved histidine-rich domain, hydropathy profile, and was rich in disulfide bonds. This study showed that selenium may in discriminatively substitute S and incorporate selenium-amino acids into the desaturase that the conformation of enzyme active sites was impacted which leaded to the inhibition of the convert of linoleic acid to γ-linolenic acid and the over accumulation of linoleic acid. Selenium might enhance the fatty acid contents of fungi through influencing the desaturase structure.