Lilium Gray Mold Suppression Conferred by the Host Antimicrobial Protein LsGRP1 Involves Main Pathogen-Targeted Manipulation of the Nonantimicrobial Region LsGRP1N.

Antimicrobial protein LsGRP1 protects Lilium from gray mold mainly caused by the destructive pathogen Botrytis elliptica; however, its nonantimicrobial region LsGRP1N conversely promotes spore germination of this fungus. By assaying the effects of LsGRP1N, LsGRP1, and the combination of LsGRP1N and the antimicrobial region LsGRP1C on fungal spore germination, hyphal growth, and Lilium gray mold development, LsGRP1N was found to improve the LsGRP1C sensitivity of B. elliptica and disease suppression by LsGRP1C. B. elliptica cell vitality assays indicated that LsGRP1N pretreatment uniquely enhanced the lethal efficiency of LsGRP1C compared to the control peptides. In addition, LsGRP1N-treated B. elliptica was demonstrated to lower infection-related gene expression and increase host-defense-eliciting activity, as indicated by reverse transcription quantitative polymerase chain reaction and histochemical-staining-based callose detection results, respectively. Therefore, LsGRP1N showed a novel mode of action for antimicrobial proteins by manipulating the main pathogen, which facilitated the development of target-specific and dormant microbe-eradicating antimicrobial agents.

LsGRP1, a class II glycine-rich protein of Lilium, confers plant resistance via mediating innate immune activation and inducing fungal programmed cell death.

Defence-related LsGRP1 is a leaf-specific plant class II glycine-rich protein (GRP) involved in salicylic acid-induced systemic resistance against grey mould caused by necrotrophic Botrytis elliptica in lily (Lilium) cultivar Stargazer. The C-terminal region of LsGRP1 (LsGRP1C ) can inhibit fungal growth in vitro via a mechanism of inducing fungal apoptosis programmed cell death (PCD). In this study, the role of LsGRP1 in induced defence mechanism was investigated using LsGRP1-silenced Stargazer lily and LsGRP1-transgenic Arabidopsis thaliana. LsGRP1 silencing in lily was found to slightly inhibit plant growth and greatly increase the susceptibility to B. elliptica by suppressing callose deposition and early reactive oxygen species (ROS) accumulation. In contrast, LsGRP1-transgenic Arabidopsis showed higher resistance to Botrytis cinerea and also to Pseudomonas syringae pv. tomato DC3000 as compared to the wild type, accompanied with the enhancement of callose deposition and ROS accumulation. Additionally, LsGRP1 silencing increased plant cell death caused by B. elliptica secretion and reduced pathogen-associated molecular pattern (PAMP)-triggered defence activation in Stargazer lily. Consistently, LsGRP1 expression boosted PAMP-triggered defence responses and effector recognition-induced hypersensitive response in Arabidopsis. Moreover, fungal apoptosis PCD triggered by LsGRP1 in an LsGRP1C -dependent manner was demonstrated by leaf infiltration with LsGRP1C -containing recombinant proteins in Stargazer lily. Based on these results, we presume that LsGRP1 plays roles in plant defence via functioning as a pathogen-inducible switch for plant innate immune activation and acting as a fungal apoptosis PCD inducer to combat pathogen attack.

The effect of yoga on sleep quality and insomnia in women with sleep problems: a systematic review and meta-analysis.

BACKGROUND: To examine the effectiveness and safety of yoga of women with sleep problems by performing a systematic review and meta-analysis. METHODS: Medline/PubMed, ClinicalKey, ScienceDirect, Embase, PsycINFO, and the Cochrane Library were searched throughout the month of June, 2019. Randomized controlled trials comparing yoga groups with control groups in women with sleep problems were included. Two reviewers independently evaluated risk of bias by using the risk of bias tool suggested by the Cochrane Collaboration for programming and conducting systematic reviews and meta-analyses. The main outcome measure was sleep quality or the severity of insomnia, which was measured using subjective instruments, such as the Pittsburgh Sleep Quality Index (PSQI), Insomnia Severity Index (ISI), or objective instruments such as polysomnography, actigraphy, and safety of the intervention. For each outcome, a standardized mean difference (SMD) and confidence intervals (CIs) of 95% were determined. RESULTS: Nineteen studies in this systematic review included 1832 participants. The meta-analysis of the combined data conducted according to Comprehensive Meta-Analysis showed a significant improvement in sleep (SMD = - 0.327, 95% CI = - 0.506 to - 0.148, P < 0.001). Meta-analyses revealed positive effects of yoga using PSQI scores in 16 randomized control trials (RCTs), compared with the control group in improving sleep quality among women using PSQI (SMD = - 0.54; 95% CI = - 0.89 to - 0.19; P = 0.003). However, three RCTs revealed no effects of yoga compared to the control group in reducing insomnia among women using ISI (SMD = - 0.13; 95% CI = - 0.74 to 0.48; P = 0.69). Seven RCTs revealed no evidence for effects of yoga compared with the control group in improving sleep quality for women with breast cancer using PSQI (SMD = - 0.15; 95% CI = - 0.31 to 0.01; P = 0.5). Four RCTs revealed no evidence for the effects of yoga compared with the control group in improving the sleep quality for peri/postmenopausal women using PSQI (SMD = - 0.31; 95% CI = - 0.95 to 0.33; P = 0.34). Yoga was not associated with any serious adverse events. DISCUSSION: This systematic review and meta-analysis demonstrated that yoga intervention in women can be beneficial when compared to non-active control conditions in term of managing sleep problems. The moderator analyses suggest that participants in the non-breast cancer subgroup and participants in the non-peri/postmenopausal subgroup were associated with greater benefits, with a direct correlation of total class time with quality of sleep among other related benefits.

Correction to: Prokaryotic expression and action mechanism of antimicrobial LsGRP1C recombinant protein containing a fusion partner of small ubiquitin-like modifier.

The published online version contains editing mistake in Table 2. See below for the corrected Table.

Prokaryotic expression and action mechanism of antimicrobial LsGRP1C recombinant protein containing a fusion partner of small ubiquitin-like modifier.

Antimicrobial peptides (AMPs) are peptides exhibiting broad-spectrum antimicrobial activities and considered as potential therapeutic agents. LsGRP1C, a novel AMP derived from defense-related LsGRP1 protein of Lilium, was proven to inhibit kinds of bacteria and fungi via alteration of microbial membrane permeability and induction of fungal programmed cell death-like phenomena by in vitro assays using synthetic LsGRP1C. In this study, the prokaryotic production of LsGRP1C recombinant protein containing an N-terminal fusion partner of the yeast small ubiquitin-like modifier (SUMO) was achieved by using optimized Escherichia coli host and purification buffer system, which lead to a high yield of soluble SUMO-LsGRP1C fusion protein. In vitro assay revealed that E. coli-expressed SUMO-LsGRP1C exhibited even better antifungal activity as compared to synthetic LsGRP1C. Meanwhile, the ability of SUMO-LsGRP1C in conducting fungal membrane permeabilization and programmed cell death was verified by SYTOX Green staining and 4',6-diamidino-2-phenylindole staining/terminal deoxynucleotidyl transferase dUTP nick-end labeling assays, respectively, indicating that E. coli-expressed SUMO-LsGRP1C shares identical modes of action with synthetic LsGRP1C. Herein, this E. coli expression system enables the effective and convenient production of antimicrobial LsGRP1C in a form of SUMO-fused recombinant protein.