Batch Transduction of Transposon Mutant Libraries for Rapid Phenotype Screening in Staphylococcus

Author(s):  
Katherine L. Maliszewski
Keyword(s):  
Author(s):  
Duarte Barros ◽  
Flávia Borges-Machado ◽  
Wagner Andrade da Silva ◽  
Alinne Nascimento ◽  
Joana Carvalho ◽  
...  

2011 ◽  
Vol 3 (8) ◽  
pp. 451-464 ◽  
Author(s):  
Wendy WeiJia Soon ◽  
Lance David Miller ◽  
Michael A. Black ◽  
Cyril Dalmasso ◽  
Xiu Bin Chan ◽  
...  

Foods ◽  
2021 ◽  
Vol 10 (10) ◽  
pp. 2454
Author(s):  
Rebecca N. Bland ◽  
Jared D. Johnson ◽  
Joy G. Waite-Cusic ◽  
Alexandra J. Weisberg ◽  
Elizabeth R. Riutta ◽  
...  

Recent listeriosis outbreaks linked to fresh produce suggest the need to better understand and mitigate L. monocytogenes contamination in packing and processing environments. Using whole genome sequencing (WGS) and phenotype screening assays for sanitizer tolerance, we characterized 48 L. monocytogenes isolates previously recovered from environmental samples in five produce handling facilities. Within the studied population there were 10 sequence types (STs) and 16 cgMLST types (CTs). Pairwise single nucleotide polymorphisms (SNPs) ranged from 0 to 3047 SNPs within a CT, revealing closely and distantly related isolates indicative of both sporadic and continuous contamination events within the facility. Within Facility 1, we identified a closely related cluster (0–2 SNPs) of isolates belonging to clonal complex 37 (CC37; CT9492), with isolates recovered during sampling events 1-year apart and in various locations inside and outside the facility. The accessory genome of these CC37 isolates varied from 94 to 210 genes. Notable genetic elements and mutations amongst the isolates included the bcrABC cassette (2/48), associated with QAC tolerance; mutations in the actA gene on the Listeria pathogenicity island (LIPI) 1 (20/48); presence of LIPI-3 (21/48) and LIPI-4 (23/48). This work highlights the potential use of WGS in tracing the pathogen within a facility and understanding properties of L. monocytogenes in produce settings.


2020 ◽  
Vol 70 (11) ◽  
pp. 1914-1925
Author(s):  
Abderahim Gaceb ◽  
Marco Barbariga ◽  
Gesine Paul

Abstract Parkinson’s disease (PD) is characterised by the progressive degeneration of dopaminergic (DA) neurons in the substantia nigra pars compacta. Post-mortem data suggests that the loss of DA markers may long precede the cell death, leaving a window to rescue the DA phenotype. Screening for potential neuroprotective or restorative therapies, however, requires that partial lesions of DA neurons can be modelled in vitro. In order to establish a partial lesion model of DA neurons in vitro, we evaluated the effects of different exposure times to 1-methyl-4-phenylpyridinium (MPP+) and 6-hydroxydopamine (6-OHDA) on the cell survival and DA marker expression using DA neurons derived from the Lund human mesencephalic (LUHMES) cell line. We show that 24-h incubation with 50 μM of MPP+ or 6-h incubation with 100 μM of 6-OHDA leads to a significant decrease in the protein expression of DA markers without affecting overall cell death, consistent with a mild DA lesion. Using conditioned medium of human brain–derived pericytes stimulated with platelet-derived growth factor BB (PDGF-BB), we demonstrate a significant upregulation of DA markers. In conclusion, we provide an experimental model of an in vitro DA neuron partial lesion suitable to study different molecules and their potential neuroprotective or neurorestorative effects on the DA phenotype. We provide evidence that the secretome of brain pericytes stimulated via PDGF-BB/PDGFRβ affects DA marker expression and may represent one possible mechanism contributing to the neurorestoration previously observed in PD by this growth factor.


2016 ◽  
Vol 131 ◽  
pp. 113-121 ◽  
Author(s):  
Mary E. Walter ◽  
Alicia Ortiz ◽  
Casey Sondgeroth ◽  
Nathan M. Sindt ◽  
Nikolas Duszenko ◽  
...  

Cell Cycle ◽  
2007 ◽  
Vol 6 (18) ◽  
pp. 2276-2283 ◽  
Author(s):  
Richard O. Burney ◽  
Alan I. Lee ◽  
Denise E. Leong ◽  
Joshua T. Jones ◽  
Angela T. Hahn ◽  
...  

2006 ◽  
Vol 17 (4) ◽  
pp. 288-297 ◽  
Author(s):  
Keith A. Ching ◽  
Michael P. Cooke ◽  
Lisa M. Tarantino ◽  
Hilmar Lapp

2019 ◽  
Vol 15 (2) ◽  
pp. 90-94
Author(s):  
Mohanasudnari SK ◽  
Padmaja A

Abstract: Frailty refers to a loss of physiologic function that makes a person susceptible to disability from minor stresses. The frailty syndrome is a collection of symptoms primarily due to the aging-related loss and dysfunction of skeletal muscle and bone, that place older adults at increased levels of risk for disability, dependency, falls, injury, ospitalization, need for long term care, and mortality. Frailty is thought distinguishable from disability and comorbidity. Frailty always implies multisystem dysfunction. Severity of frailty range subclinical to a clinical stage to impending death. It is Important to recognize and treat the frailty syndrome before occurrence of any adverse outcomes. Fried's Phenotype screening tool identifies a person as being frail


2021 ◽  
pp. 030098582110305
Author(s):  
Peter Vogel ◽  
Robert W. Read ◽  
Gwenn M. Hansen ◽  
David R. Powell

The development of mouse models that replicate the genetic and pathological features of human disease is important in preclinical research because these types of models enable the completion of meaningful pharmacokinetic, safety, and efficacy studies. Numerous relevant mouse models of human disease have been discovered in high-throughput screening programs, but there are important specific phenotypes revealed by histopathology that are not reliably detected by any other physiological or behavioral screening tests. As part of comprehensive phenotypic analyses of over 4000 knockout (KO) mice, histopathology identified 12 lines of KO mice with lesions indicative of an autosomal recessive myopathy. This report includes a brief summary of histological and other findings in these 12 lines. Notably, the inverted screen test detected muscle weakness in only 4 of these 12 lines ( Scyl1, Plpp7, Chkb, and Asnsd1), all 4 of which have been previously recognized and published. In contrast, 6 of 8 KO lines showing negative or inconclusive findings on the inverted screen test ( Plppr2, Pnpla7, Tenm1, Srpk3, Sidt2, Yif1b, Mrs2, and Pnpla2) had not been previously identified as having myopathies. These findings support the need to include histopathology in phenotype screening protocols in order to identify novel genetic myopathies that are not clinically evident or not detected by the inverted screen test.


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