The Gain-of-Function Mutation, OsSpl26, Positively Regulates Plant Immunity in Rice.

Rice spotted-leaf mutants are ideal materials to study the molecular mechanism underlying programmed cell death and disease resistance in plants. LOC_Os07g04820 has previously been identified as the candidate gene responsible for the spotted-leaf phenotype in rice Spotted-leaf 26 (Spl26) mutant. Here, we cloned and validated that LOC_Os07g04820 is the locus controlling the spotted-leaf phenotype of Spl26 by reverse functional complementation and CRISPR/Cas9-mediated knockout of the mutant allele. The recessive wild-type spl26 allele (Oryza sativa spotted-leaf 26, Osspl26) is highly conservative in grass species and encodes a putative G-type lectin S-receptor-like serine/threonine protein kinase with 444 amino acid residuals. OsSPL26 localizes to the plasma membrane and can be detected constitutively in roots, stems, leaves, sheaths and panicles. The single base substitution from T to A at position 293 leads to phenylalanine/tyrosine replacement at position 98 in the encoded protein in the mutant and induces excessive accumulation of H2O2, leading to oxidative damage to cells, and finally, formation of the spotted-leaf phenotype in Spl26. The formation of lesions not only affects the growth and development of the plants but also activates the defense response and enhances the resistance to the bacterial blight pathogen, Xanthomonas oryzae pv. oryzae. Our results indicate that the gain-of-function by the mutant allele OsSpl26 positively regulates cell death and immunity in rice.

The OsABCI7 Transporter Interacts with OsHCF222 to Stabilize the Thylakoid Membrane in Rice.

The thylakoid membrane is a highly complex membrane system in plants and plays crucial roles in the biogenesis of the photosynthetic apparatus and plant development. However, the genetic factors involved in chloroplast development and its relationship with intracellular metabolites are largely unknown. Here, a rice (Oryza sativa) chlorotic and necrotic leaf1 (cnl1) mutant was identified and map-based cloning revealed that a single base substitution followed by a 6-bp deletion in the ATP-binding cassette transporter I family member7 (OsABCI7) resulted in chlorotic and necrotic leaves with thylakoid membrane degradation, chlorophyll breakdown, photosynthesis impairment, and cell death in cnl1 Furthermore, the expression of OsABCI7 was inducible under lower temperatures, which severely affected cnl1 chloroplast development, and etiolated cnl1 seedlings were unable to recover to a normal green state under light conditions. Functional complementation and overexpression showed that OsABCI7 could rescue the cnl1 chlorotic and necrotic phenotype. OsABCI7 interacted with HIGH CHLOROPHYLL FLUORESCENCE222 (OsHCF222) to regulate cellular reactive oxygen species (ROS) homeostasis for thylakoid membrane stability. OsABCI7 localized to thylakoid membranes, while OsHCF222 targeted to endoplasmic reticulum and chloroplasts. Exogenous application of ascorbic acid eased the yellowish leaf phenotype by increasing chlorophyll content and alleviating ROS stress in cnl1 Unlike cnl1, the CRISPR/Cas9-mediated OsHCF222 knockout lines showed chlorotic leaves but were seedling lethal. Our results provide insight into the functions of ABC transporters in rice, especially within the relationship between ROS homeostasis and stability of thylakoid membranes.

Room Temperature Strengthening and High-Temperature Superplasticity of Mg-Li-Al-Sr-Y Alloy Fabricated by Asymmetric Rolling and Friction Stir Processing.

Magnesium-lithium alloy is the lightest alloy to date. To explore its room temperature strength and high-temperature ductility, a plate of a new fine-grained Mg-9.13Li-3.74Al-0.31Sr-0.11Y alloy was fabricated by asymmetric rolling, and the rolled plate was subjected to friction stir processing (FSP). The microstructure and mechanical properties at room and elevated temperatures were investigated by optical microscopy, X-ray diffraction (XRD), energy dispersive spectroscopy (EDS), and tensile tester. Grain refinement with an average grain size in the α-Mg phase of 1.65 µm and an average grain size in the ß-Li phase of 4.24 µm was achieved in the water-cooled FSP alloy. For room temperature behavior, the ultimate tensile strength of 208 ± 4 MPa, yield strength of 193 ± 2 MPa, and elongation of 48.2% were obtained in the water-cooled FSP alloy. XRD and EDS analyses revealed that the present alloy consists of α-Mg and ß-Li phases, Al2Y, Al4Sr, MgLi2Al, and AlLi intermetallic compounds. For high-temperature behavior, the maximum superplasticity or ductility of 416% was demonstrated in this fine-grained alloy with an average grain size of 10 µm at 573 K and 1.67 × 10-3 s-1. A power-law constitutive equation was established. The stress exponent was 2.29 (≈2) (strain rate sensitivity 0.44), and the deformation activation energy was 162.02 kJ/mol. This evidence confirmed that the dominant deformation mechanism at elevated temperatures is grain boundary and interphase boundary sliding controlled by lattice diffusion.

High Strain Rate Quasi-Superplasticity Behavior in an Ultralight Mg-9.55Li-2.92Al-0.027Y-0.026Mn Alloy Fabricated by Multidirectional Forging and Asymmetrical Rolling.

To explore new approaches to severe plastic deformation and the ductility of a multicomponent magnesium-lithium alloy, an ultralight microduplex Mg-9.55Li-2.92Al-0.027Y-0.026Mn alloy was made by novel multidirectional forging and asymmetrical rolling, and the superplasticity behavior was investigated by optical microscope, hot tensile test, and modeling. The average grain size is 1.9 µm in this alloy after multidirectional forging and asymmetrical rolling. Remarkable grain refinement caused by such a forming, which turns the as-cast grain size of 144.68 µm into the as-rolled grain size of 1.9 µm, is achieved. The elongation to failure of 228.05% is obtained at 523 K and 1 × 10-2 s-1, which demonstrates the high strain rate quasi-superplasticity. The maximum elongation to failure of 287.12% was achieved in this alloy at 573 K and 5 × 10-4 s-1. It was found that strain-induced grain coarsening at 523 K is much weaker than the strain-induced grain coarsening at 573 K. Thus, the ductility of 228.05% is suitable for application in high strain rate superplastic forming. The stress exponent of 3 and the average activation energy for deformation of 50.06 kJ/mol indicate that the rate-controlling deformation mechanism is dislocation-glide controlled by pipe diffusion.

Association of polymorphisms in TLR2 and TLR4 with asthma risk: An update meta-analysis.

BACKGROUND: Several epidemiological studies have focused on the association between polymorphisms in toll-like receptors (TLRs) and asthma. However, the results remained inconclusive. METHODS: We systematically reviewed the database of PubMed, EMBASE, Web of Science, CNKI, and Google scholar for all related articles on TLR polymorphisms and asthma. We used the software STATA 12.0 to conduct the meta-analysis. The heterogeneity and publication bias were examined, respectively. RESULTS: Eighteen studies consisting of 3538 asthma cases and 4090 controls were selected into the meta-analysis. The pooled odds ratios (ORs) show that rs3804099 was associated with asthma in dominant model (OR = 1.51, 95% CI = 1.17-1.96, P = .002), and rs4986791 was associated with asthma in additive model (OR = 0.81, 95% CI = 0.64-1.02, P = .07) and dominant model (OR = 0.76, 95% CI = 0.60-0.97, P = .025). CONCLUSION: The combined results show that rs3804099 in TLR2 and rs4986791 in TLR4 were significantly associated with asthma risk. Polymorphisms in TLRs play important roles in asthma.

Quercetin induces autophagy via FOXO1-dependent pathways and autophagy suppression enhances quercetin-induced apoptosis in PASMCs in hypoxia.

Quercetin, an important dietary flavonoid has been demonstrated to potentially reverse or even prevent pulmonary arterial hypertension (PAH) progression. However, the effects of quercetin on apoptosis and autophagy in pulmonary arterial smooth muscle cells (PASMCs) have not yet been clearly elucidated. The current study found that quercetin significantly induce the apoptotic and autophagic capacities of PASMCs in vitro and in vivo in hypoxia. In addition, we found that quercetin increases FOXO1 (a major mediator in autophagy regulation) expression and transcriptional activity. Moreover, FOXO1 knockdown by siRNAs inhibited the phosphorylation of mTOR and 4E-BPI, which is downstream of P70-S6K, and markedly blocked quercetin-induced autophagy. We also observed that FOXO1-mediated autophagy was achieved via SESN3 not Rictor upregulation and after mTOR suppression. Furthermore, Treatment with autophagy-specific inhibitors could markedly enhance quercetin-induced apoptosis in PASMCs under hypoxia. Finally, quercetin in combination with autophagy inhibition treatment could enhance the therapeutic effects of quercetin in hypoxia-associated PAH in vivo. Taken together, quercetin could enhance hypoxia-induced autophagy through the FOXO1-SENS3-mTOR pathway in PASMCs. Combining quercetin and autophagy inhibitors may be a novel therapeutic strategy for treating hypoxia-associated PAH.