Exemplar Abstract for Kocuria rhizophila Kovács et al. 1999.

2003 ◽  
Author(s):  
Charles Thomas Parker ◽  
Dorothea Taylor ◽  
George M Garrity
Keyword(s):  
2003 ◽  
Author(s):  
Charles Thomas Parker ◽  
George M Garrity
Keyword(s):  

2018 ◽  
Vol 09 (01) ◽  
Author(s):  
Anthony Nguyen ◽  
Randall Zain Allison ◽  
Ken Maynard ◽  
Joel Patterson

2020 ◽  
Vol 28 (3) ◽  
pp. 169-170
Author(s):  
Vincent Mathy ◽  
Benjamin Chousterman ◽  
Anne-Lise Munier ◽  
Emmanuelle Cambau ◽  
Hervé Jacquier ◽  
...  

2020 ◽  
Author(s):  
J. Amaranath Govindan ◽  
Elamparithi Jayamani ◽  
Victor Lelyveld ◽  
Jack Szostak ◽  
Gary Ruvkun

AbstractMicrobial toxins and virulence factors often target the eukaryotic translation machinery. Caenorhabditis elegans surveils for such microbial attacks by monitoring translational competence, and if a deficit is detected, particular drug detoxification and bacterial defense genes are induced. The bacteria Kocuria rhizophila has evolved countermeasures to animal translational surveillance and defense pathways. Here, we used comprehensive genetic analysis of Kocuria rhizophila to identify the bacterial genetic pathways that inhibit C. elegans translational toxin surveillance and defense. Kocuria rhizophila mutations that disrupt its ability to disable animal immunity and defense map to multiple steps in the biosynthesis of a 50-carbon bacterial carotenoid from 5 carbon precursors. Extracts of the C50 carotenoid from wild type K. rhizophila could restore this bacterial anti-immunity activity to K. rhizophila carotenoid biosynthetic mutant. Corynebacterium glutamicum, also inhibits the C. elegans translation detoxification response by producing the C50 carotenoid decaprenoxanthin, and C. glutamicum carotenoid mutants are defective in this suppression of C. elegans detoxification. Consistent with the salience of these bacterial countermeasures to animal drug responses, bacterial carotenoids sensitize C. elegans to drugs that target translation and inhibit food aversion behaviors normally induced by protein translation toxins or mutations. The surveillance and response to toxins is mediated by signaling pathways conserved across animal phylogeny, suggesting that these bacterial carotenoids may also suppress such human immune and toxin responses.


2010 ◽  
Vol 60 (4) ◽  
pp. 914-918 ◽  
Author(s):  
Eun-Jin Park ◽  
Min-Soo Kim ◽  
Seong Woon Roh ◽  
Mi-Ja Jung ◽  
Jin-Woo Bae

A novel actinobacterium, strain P30T, was isolated from jeotgal, a traditional Korean fermented seafood. Cells were aerobic, Gram-positive, non-motile and coccoid. Optimal growth occurred at 30–37 °C, at pH 8–9 and in the presence of 0–2 % (w/v) NaCl. Based on 16S rRNA gene sequence analysis, strain P30T was phylogenetically closely related to Kocuria carniphila, Kocuria gwangalliensis, Kocuria rhizophila, Kocuria marina, Kocuria rosea and K. varians with levels of similarity of 98.6, 98.2, 98.1, 97.4, 97.3 and 97.3 %, respectively, to the type strains of these species. Levels of DNA–DNA relatedness between strain P30T and the type strains of K. carniphila, K. rhizophila, K. marina, K. rosea and K. varians were 37, 43, 37, 25 and 17 %, respectively. The predominant menaquinone of strain P30T was MK-7. Major cellular fatty acids were anteiso-C15 : 0, iso-C15 : 0 and iso-C16 : 0. The genomic DNA G+C content of strain P30T was 70.2 mol%. Based on these data, strain P30T is considered to represent a novel species of the genus Kocuria, for which the name Kocuria atrinae sp. nov. is proposed. The type strain is P30T (=KCTC 19594T=JCM 15914T).


2020 ◽  
Vol 89 (2) ◽  
pp. 201-208
Author(s):  
Pavlína Navrátilová ◽  
Jana Vyhnálková ◽  
Hana Zachovalová ◽  
Lenka Vorlová

The aim of this study was to determine the detection capability (CCβ) of a multi-plate diffusion method for selected cephalosporins for which the maximum residue limits (MRLs) in milk have been set (ceftiofur, cefoperazone, cephalexine, cephazoline, cephalonium, cephapirine, cefquinome). The multiplate method was composed of Bacillus subtilis BGA CCM 4062 plates (agar pH of 6, 8 and 7.2); Kocuria rhizophila CCM 552 plate, Geobacillus stearothermophilus CCM 5965 plate and Escherichia coli CCM 7372 plate. Geobacillus stearothermophilus plate showed the highest sensitivity. CCβ for the tested cephalosporins was determined at MRLs or lower, except for cefquinome, which was undetectable even at 12 × the MRL. Kocuria rhizophila plate showed the highest sensitivity to ceftiofur (CCβ = 100 μg/l); cephazoline and cephalonium could not be detected even at 12 × times the MRL. Escherichia coli plate was most sensitive to cefoperazone (CCβ = 60 μg/l). Other than cephapirine, none of the cephalosporins could be detected by B. subtilis BGA (pH 6, 8 and 7.2) plates even at 12 × the MRL. Our results demonstrate the differences in sensitivity to selected cephalosporins of the individual plate methods that together form the multi-plate method. The multi-plate method is sensitive enough to detect most of the tested cephalosporins, with the exception of cefquinome, which could not be detected at levels close to MRL.


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