Identification and Characterization of Pheromone Receptors and Interplay between Receptors and Pheromone Binding Proteins in the Diamondback Moth,Plutella xyllostella

Moths depend on olfactory cues such as sex pheromones to find and recognize mating partners. Pheromone receptors (PRs) and Pheromone binding proteins (PBPs) are thought to be associated with olfactory signal transduction of pheromonal compounds in peripheral olfactory reception. Here six candidate pheromone receptor genes in the diamondback moth, Plutella xyllostella were identified and cloned. All of the six candidate PR genes display male-biased expression, which is a typical characteristic of pheromone receptors. In the Xenopus-based functional study and in situ hybridization, PxylOR4 is defined as another pheromone receptor in addition to the previously characterized PxylOR1. In the study of interaction between PRs and PBPs, PxylPBPs could increase the sensitivity of the complex expressing oocyte cells to the ligand pheromone component while decreasing the sensitivity to pheromone analogs. We deduce that activating pheromone receptors in olfactory receptor neurons requires some role of PBPs to pheromone/PBP complex. If the chemical signal is not the pheromone component, but instead, a pheromone analog with a similar structure, the complex would have a decreased ability to activate downstream pheromone receptors.     

Expanding the scope of genome editing with SpG and SpRY variants in rice

正Dear Editor,The clustered regularly interspaced short palindromic repeats/CRISPR-associated nuclease 9 (CRISPR/Cas9) system, since it was excavated, has been rapidly developed and sparked a revolution in the genome editing field. In principle,CRISPR/Cas9 system relies on the recognition of specific loci on the genome, which is titled the protospacer adjacent motif (PAM). However, the canonical Streptococcus pyogenes Cas9 (SpCas9) nuclease only recognizes NGG or NAG PAMs, rendering an inherent obstacle in amplifying the application of CRISPR/Cas9 technology.     

LncRNA MIR155HG Promotes Temozolomide Resistance by Activating the Wnt/β-Catenin Pathway Via Binding to PTBP1 in Glioma

Temozolomide (TMZ) is widely used for glioma therapy in the clinic. Currently, the development of TMZ resistance has largely led to poor prognosis. However, very little is understood about the role of MIR155HG, as a long noncoding RNA, in TMZ resistance. In our study, MIR155HG level was markedly higher in glioma patients than in normal controls and that poor survival was positively correlated with MIR155HG expression. It was apparent that TMZ sensitivity was promoted by downregulation of MIR155HG, and this could be reversed by MIR155HG overexpression in vivo and in vitro. Furthermore, polypyrimidine tract binding protein 1 (PTBP1) was proven to bind with MIR155HG and to regulate MIR155HG-related TMZ resistance. Mechanistic investigation showed that the expression levels of both MIR155HG and PTBP1 influenced the expression of relevant proteins in the Wnt/β-catenin pathway. Collectively, the study demonstrated that the knockdown of MIR155HG increased glioma sensitivity to TMZ by inhibiting Wnt/β-catenin pathway activation via potently downregulating PTBP1.

     

Generation of marker-free transgenic rice using CRISPR/Cas9 system controlled by ?oral speci?c promoters

Recently, the CRISPR/Cas9 system has been used as a powerful tool for genome editing in many species (Jinek et al., 2012;Cong et al., 2013;Wright et al., 2016;Li et al., 2017;Deng et al., 2018). The CR1SPR/Cas9 system can not only be used as a useful technology to disrupt endogenous genes but also expand numerous other applications, such as precise base editing (Komor et al., 2016;Zong et al., 2017), regulation of gene expression (Gilbert et al., 2013), and gene replacement or insertion (Wang et al., 2017).     

广西唇形科植物新记录

该文首次报道了唇形科5种植物在广西的新记录——簇序属(Craniotome Reichenb.)及簇序草[Craniotome furcata(Link)Kuntze]、西南水苏[Stachys kouyangensis(Vaniot)Dunn]、海南深红鸡脚参[Orthosiphon rubicundus(D.Don)Benth.var.hainanensis Sun ex C.Y.Wu]、黄花香薷[Elsholtzia flava(Benth.)Benth.]、滨海白绒草[Leucas chinensis(Retz.)R.Br.]。引证标本均存放于广西中医药研究院标本馆(GXMI)。     

Specific loops D,E and F of nicotinic acetylcholine receptor β1 subunit may confer imidacloprid selectivity between Myzus persicae and its predatory enemy Pardosa pseudoannulata

One nicotinic acetylcholine receptor non-α subunit was cloned from the pond wolf spider, Pardosa pseudoannulata, an important predatory enemy of some insect pests with agricultural importance, such as the green peach aphid Myzus persicae. The subunit shows high amino acid identities to insect β1 subunits (74–78%), and was denoted as Ppβ1. Although high identities are found between Ppβ1 and insect β1 subunits, amino acid differences are found within loops D, E and F, important segments contributing to ligand binding. The effects of amino acid differences within these loops were evaluated by introducing loops of insect or spider β1 subunits into rat β2 subunit and co-expressing with insect α subunit. The corresponding regions of rat β2 chimera β2^Mpβ1 (β2 with loops D, E and F from M. persicae β1 subunit Mpβ1) were replaced by loops D, E and F of Ppβ1 singly or together to construct different chimeras. When these chimeras were co-expressed with insect Nlα1, it was found that the replacement of loops D, E and F of β2^Mpβ1 by that of Ppβ1 resulted in a right-ward shift of the imidacloprid dose–response curves, reflecting increases in EC₅₀, compared to Nlα1/β2^Mpβ1. By contrast, the influences on ACh potency were minimal. The further study showed that R81Q, N137G and F190W differences, within loops D, E and F respectively, contributed mainly to these sensitivity changes. This study contributes to our understanding of the molecular mechanism underlying selectivity of neonicotinoids against insects over spiders.     

Exploring off-targets and off-systems for adverse drug reactions via chemical-protein interactome--clozapine-induced agranulocytosis as a case study

In the era of personalized medical practice, understanding the genetic basis of patient-specific adverse drug reaction (ADR) is a major challenge. Clozapine provides effective treatments for schizophrenia but its usage is limited because of life-threatening agranulocytosis. A recent high impact study showed the necessity of moving clozapine to a first line drug, thus identifying the biomarkers for drug-induced agranulocytosis has become important. Here we report a methodology termed as antithesis chemical-protein interactome (CPI), which utilizes the docking method to mimic the differences in the drug-protein interactions across a panel of human proteins. Using this method, we identified HSPA1A, a known susceptibility gene for CIA, to be the off-target of clozapine. Furthermore, the mRNA expression of HSPA1A-related genes (off-target associated systems) was also found to be differentially expressed in clozapine treated leukemia cell line. Apart from identifying the CIA causal genes we identified several novel candidate genes which could be responsible for agranulocytosis. Proteins related to reactive oxygen clearance system, such as oxidoreductases and glutathione metabolite enzymes, were significantly enriched in the antithesis CPI. This methodology conducted a multi-dimensional analysis of drugs' perturbation to the biological system, investigating both the off-targets and the associated off-systems to explore the molecular basis of an adverse event or the new uses for old drugs.     

Sodium selenite-induced activation of DAPK promotes autophagy in human leukemia HL60 cells

Autophagy has been suggested as a possible mechanism for non-apoptotic death despite evidence from many species that autophagy represents a survival strategy of cells under stress. From our previous findings that supranutritional doses of sodium selenite induced apoptosis in human leukemia cells, now we show autophagic cell death occurred after selenite exposure in HL60, suggested an alternative mechanism for the potential therapeutic properties of selenite. Additionally, Death-associated Protein Kinase (DAPK) performed a significantly increased expression during this process, concomitantly with gradually decreased phosphorylation at Ser(308). We further reveal that the up-regulation of DAPK which depends on selenite-activated ERK had no effect on autophagy. However, activation of DAPK via PP2A-mediated dephosphorylation at Ser(308) serves as a new strategy for autophagy induction. In conclusion, these results indicate that PP2A-mediated activated DAPK sensitizes HL60 cells to selenite, ultimately triggers autophagic cell death pathway to commit cell demise. [BMB reports 2012; 45(3): 194-199].