松油烯-４-醇对粘虫幼虫的生物活性

测定了杀虫植物砂地柏Sabina vulgaris Ant.的精油中主杀虫成分-松油烯-4-醇（terpinen 4.01）对粘虫Mythimna separata Walker幼虫的生物活性。结果表明,松油烯- 4-醇对粘虫主要表现为熏蒸作用,对粘虫3龄幼虫24 h的熏蒸LC₅₀为5.3473 μL/L ;还具一定触杀作用,对粘虫4龄幼虫24 h的LD₅₀为147.8 μg/虫。试虫的中毒症状可明显地分为兴奋、痉挛、麻痹和死亡4个阶段,而麻痹的部分试虫有复苏现象。可明显抑制Na⁺ ,K⁺ATP酶的活性,在兴奋期、痉挛期、麻痹期和复苏期,抑制率介于21.28%～34.92% 之间。离体条件下对Na⁺,K⁺ATP酶的I₅₀为133.75 μg·mL^-1;对AChE活性有一定的影响;对酯酶,在兴奋期,酶活力为对照的7.0%,在麻痹期则为对照的1.33倍,而复苏期试虫的酯酶活力与对照相当。     

Elicitor hydrophobin Hyd1 interacts with Ubiquilin1‐like to induce maize systemic resistance

Trichoderma harzianum is a plant-beneficial fungus that secretes small cysteine-rich proteins that induce plant defense responses; however, the molecular mechanism involved in this induction is largely unknown.Here, we report that the class II hydrophobin Th Hyd1 acts as an elicitor of induced systemic resistance(ISR) in plants. Immunogold labeling and immunofluorescence revealed Th Hyd1 localized on maize(Zea mays) root cell plasma membranes. To identify host plant protein interactors of Hyd1, we screened a maize B73 root c DNA library. Th Hyd1 interacted directly with ubiquilin1-like(UBL). Furthermore, the N-terminal fragment of UBL was primarily responsible for binding with Hyd1 and the eight-cysteine amino acid of Hyd1 participated in the protein-protein interactions. Hyd1 from T. harzianum(Thhyd1) and ubl from maize were co-expressed in Arabidopsis thaliana, they synergistically promoted plant resistance against Botrytis cinerea. RNA-sequencing analysis of global gene expression in maize leaves 24 h after spraying with Curvularia lunata spore suspension showed that Thhyd1-induced systemic resistance was primarily associated with brassinosteroid signaling, likely mediated through BAK1. Jasmonate/ethylene(JA/ET)signaling was also involved to some extent in this response. Our results suggest that the Hyd1-UBL axis might play a key role in inducing systemic resistance as a result of Trichoderma-plant interactions.     

Comprehensive analysis of mRNA‐level and miRNA‐level subpathway activities for identifying robust ovarian cancer prognostic signatures

Ovarian cancer (OvCa) causes the highest mortality among all gynaecologic cancers. A large number of mRNA‐ or miRNA‐based signatures were identified for OvCa patient prognosis. However, the comprehensive analysis of function‐level prognostic signatures is currently not considered in OvCa. In the present study, we respectively inferred subpathway activities from mRNA and miRNA levels based on high‐throughput expression profiles and reconstructed subpathways. Firstly, the activities of two tumour pathways were calculated and the difference between normal and tumour samples were analysed using multiple tumour types. Then, we calculated subpathway activities for OvCa based on the expression profiles from both mRNA and miRNA levels. Furthermore, based on these subpathway activity matrices, we performed bootstrap analysis to obtain sub‐training sets and utilized univariate method to identify robust OvCa prognostic subpathways. A comprehensive comparison of subpathway results between these two levels was performed. As a result, we observed subpathway mutual exclusion trend between the levels of mRNA and miRNA, which indicated the necessary of combining mRNA‐miRNA levels. Finally, by using ICGC data as testing sets, we utilized two strategies to verify survival predictive power of the mRNA‐miRNA combined subpathway signatures and performed comparisons with results from individual levels. It was confirmed that our framework displayed application to identify robust and efficient prognostic signatures for OvCa, and the combined signatures indeed exhibited advantages over individual ones. In the study, we took a step forward in relevant novel integrated functional signatures for OvCa prognosis.     

Half‐Heusler Thermoelectric Module with High Conversion Efficiency and High Power Density

Half‐Heusler (HH) compounds have shown great potential in waste heat recovery. Among them, p‐type NbFeSb and n‐type ZrNiSn based alloys have exhibited the best thermoelectric (TE) performance. However, TE devices based on NbFeSb‐based HH compounds are rarely studied. In this work, bulk volumes of p‐type (Nb_0.8Ta_0.2)_0.8Ti_0.2FeSb and n‐type Hf_0.5Zr_0.5NiSn_0.98Sb_0.02 compounds are successfully prepared with good phase purity, compositional homogeneity, and matchable TE performance. The peak zTs are higher than 1.0 at 973 K for Hf_0.5Zr_0.5NiSn_0.98Sb_0.02 and at 1200 K for (Nb_0.8Ta_0.2)_0.8Ti_0.2FeSb. Based on an optimal design by a full‐parameters 3D finite element model, a single stage TE module with 8 n‐p HH couples is assembled. A high conversion efficiency of 8.3% and high power density of 2.11 W cm^?2 are obtained when hot and cold side temperatures are 997 and 342 K, respectively. Compared to the previous TE module assembled by the same materials, the conversion efficiency is enhanced by 33%, while the power density is almost the same. Given the excellent mechanical robustness and thermal stability, matchable thermal expansion coefficient and TE properties of NbFeSb and ZrNiSn based HH alloys, this work demonstrates their great promise for power generation with both high conversion efficiency and high power density.     

GPI7-mediated glycosylphosphatidylinositol anchoring regulates appressorial penetration and immune evasion during infection of Magnaporthe oryzae

Glycosylphosphatidylinositol (GPI) anchoring plays key roles in many biological processes by targeting proteins to the cell wall; however, its roles are largely unknown in plant pathogenic fungi. Here, we reveal the roles of the GPI anchoring in Magnaporthe oryzae during plant infection. The GPI-anchored proteins were found to highly accumulate in appressoria and invasive hyphae. Disruption of GPI7, a GPI anchor-pathway gene, led to a significant reduction in virulence. The Δgpi7 mutant showed significant defects in penetration and invasive growth. This mutant also displayed defects of the cell wall architecture, suggesting GPI7 is required for cell wall biogenesis. Removal of GPI-anchored proteins in the wild-type strain by hydrofluoric acid (HF) pyridine treatment exposed both the chitin and β-1,3-glucans to the host immune system. Exposure of the chitin and β-1,3-glucans was also observed in the Δgpi7 mutant, indicating GPI-anchored proteins are required for immune evasion. The GPI anchoring can regulate subcellular localization of the Gel proteins in the cell wall for appressorial penetration and abundance of which for invasive growth. Our results indicate the GPI anchoring facilitates the penetration of M. oryzae into host cells by affecting the cell wall integrity and the evasion of host immune recognition.     

NbALY916 is involved in potato virus X P25-triggered cell death in Nicotiana benthamiana

Systemic necrosis often occurs during viral infection of plants and is thought mainly to be the result of long-term stress induced by viral infection. Potato virus X (PVX) encodes the P25 pathogenicity factor that triggers a necrotic reaction during PVX-potato virus Ysynergistic coinfection. In this study, we discovered that NbALY916, a multifunctional nuclear protein, could interact with P25. When NbALY916 expression was reduced by tobacco rattle virus (TRV)-based virus-induced gene silencing, the accumulation of P25 was increased, which would be expected to cause more severe necrosis. However, silencing of NbALY916 reduced the extent of cell death caused by P25. Furthermore, we found that overexpression of NbALY916 increased the accumulation of H₂O₂ and triggered more extensive cell death when coexpressed with P25, even though accumulation of P25 was itself reduced by the increased expression of NbALY916. Furthermore, transient expression of P25 specifically induced the expression of NbALY916 mRNA, but not the mRNAs of three other ALYs in Nicotiana benthamiana. In addition, we showed that silencing of NbALY916 or transient overexpression of NbALY916 affected the infection of PVX in N. benthamiana. Our results reveal that NbALY916 has an antiviral role that, in the case of PVX, operates by inducing the accumulation of H₂O₂ and mediating the degradation of P25.