De novo assembly of Amorpha fruticosa L. transcriptome in response to drought stress provides insight into the tolerance mechanisms

Background Amorpha fruticosa L. is a deciduous shrub that is native to North America and has been introduced to China as an ornamental plant. In order to clarify the drought resistance characteristics of Amorpha fruticosa L. and excavate the related genes involved in drought resistance regulation pathway, the mechanism of drought resistance stress of Amorpha fruticosa L. was revealed by the changes of transcriptome of Amorpha fruticosa L. under drought stress.Through the changes of the transcriptome of Amorpha fruticosa L. under drought stress, the mechanism of anti-stress of Amorpha fruticosa L. could be revealed. Methods Different concentrations of polyethylene glycol-6000 (PEG-6000) was used to simulate drought stress, and transcriptomic analysis was used to reveal the changes of gene expression patterns in Amorpha fruticosa L. seedlings. Results Results showed that Amorpha fruticosa L. seedlings were seriously affected by PEG-6000. As for the differently expressed genes (DEGs), most of them were up-regulated. The additional Go and KEGG analysis results showed that DEGs were functionally enriched in cell wall, signal transduction and hormonal regulation related pathways. DEGs like AfSOD, AfHSP, AfTGA, AfbZIP and AfGRX play roles in response to drought stress. Conclusion In conclusion, Amorpha fruticosa L. seedlings were sensitive to drought, which was different from Amorpha fruticosa L. tree, and the genes functions in drought stress responses via ABA-independent pathways. The up-regulation of Salicylic acid signal related DEGs (AfTGA and AfPR-1) indicated that Salicylic acid play a key role in response to drought stress in Amorpha fruticosa L.

De novo assembly of Amorpha fruticosa (Amorpha fruticosa L.) transcriptome in response to drought stress provides insight into the tolerance mechanisms

Background Amorpha fruticosa (Amorpha fruticosa L.) is a deciduous shrub that is native to North America and has been introduced to China as an ornamental plant.In order to cultivate drought-tolerant Amorpha fruticosa varieties, it is important to understand the drought-tolerant mechanism of Amorpha fruticosa. Through the changes of the transcriptome of Amorpha fruticosa under drought stress, the mechanism of anti-stress of Amorpha fruticosa could be revealed. Different concentrations of polyethylene glycol-6000 (PEG-6000) was used to simulate drought stress, and transcriptomic analysis was used to reveal the changes of gene expression patterns in Amorpha fruticosa seedlings.Results Results showed that Amorpha fruticosa seedlings were seriously affected by PEG-6000. As for the differently expressed genes (DEGs), most of them were up-regulated. The additional Go and KEGG analysis results showed that DEGs were functionally enriched in cell wall, signal transduction and hormonal regulation related pathways. DEGs like AfSOD, AfHSP, AfTGA, AfbZIP and AfGRX play roles in response to drought stress.Conclusion In conclusion, Amorpha fruticosa seedlings were sensitive to drought, which was different from Amorpha fruticosa tree, and the genes functions in drought stress responses via ABA‐independent pathways. The up-regulation of Salicylic acid signal related DEGs (AfTGA and AfPR-1) indicated that Amorpha fruticosa can resist drought stress through Salicylic acid.

Regulation of a Phage Endolysin by Disulfide Caging

ABSTRACT In contrast to canonical phage endolysins, which require holin-mediated disruption of the membrane to gain access to attack the cell wall, signal anchor release (SAR) endolysins are secreted by the host sec system, where they accumulate in an inactive form tethered to the membrane by their N-terminal SAR domains. SAR endolysins become activated by various mechanisms upon release from the membrane. In its inactive form, the prototype SAR endolysin, LyzP1, of coliphage P1, has an active-site Cys covalently blocked by a disulfide bond; activation involves a disulfide bond isomerization driven by a thiol in the newly released SAR domain, unblocking the active-site Cys. Here, we report that Lyz103, the endolysin of Erwinia phage ERA103, is also a SAR endolysin. Although Lyz103 does not have a catalytic Cys, genetic evidence suggests that it also is activated by a thiol-disulfide isomerization triggered by a thiol in the SAR domain. In this case, the inhibitory disulfide in nascent Lyz103 is formed between cysteine residues flanking a catalytic glutamate, caging the active site. Thus, LyzP1 and Lyz103 define subclasses of SAR endolysins that differ in the nature of their inhibitory disulfide, and Lyz103 is the first enzyme found to be regulated by disulfide bond caging of its active site.

Abstract 5765: 3T MRI Molecular Imaging of Benfluorex Treatment of Metabolic Syndrome with α v β 3 -Integrin Targeted Nanoparticles

1.5T MRI with α v β 3 -integrin targeted gadolinium nanoparticle contrast agents (NP) can detect stage I atherosclerosis in experimental animals by localizing specifically to inflammatory plaque components within minutes after injection. We hypothesized that NP could serve as an early surrogate biomarker of therapeutic efficacy for benfluorex treatment of metabolic syndrome in diabetic JCR-LA:cp rats on a 3T clinical scanner. Six week old JCR-LA:cp rats (n=6) received benfluorex in their feed (0.069% wt/wt) for 16 weeks, while control animals (n=5) received regular diet. The abdominal aorta was imaged (T1w spin echo) in 4 cross-sections at baseline and 2-hour post-injection (IV, 1.0 ml/kg NP) every 4 wks with a 3.0 T whole-body clinical MRI scanner, and total aortic wall signal was computed across all sections. Treatment of diabetic JCR-LA:cp rats with benfluorex reduced food consumption and body weight (16.0%; p<0.05); and fasting plasma insulin, leptin and triglyceride were decreased by 52.6%, 18.2% and 36.2% in treated animals. Aortic wall signal for untreated animals rose progressively, whereas signal in treated animals progressively decreased, indicative of attenuation of angiogenesis and vascular inflammation (Figure , *p<0.05). These observations represent the first report of the use of molecular imaging with an MRI surrogate biomarker at clinical field strength for quantifying therapeutic efficacy in a model of metabolic syndrome. This research has received full or partial funding support from the American Heart Association, AHA Midwest Affiliate (Illinois, Indiana, Iowa, Kansas, Michigan, Minnesota, Missouri, Nebraska, North Dakota, South Dakota & Wisconsin).