scholarly journals Spontaneous mutation accompanying decreased growth rate and cell wall thickening confers vancomycin resistance in the subpopulation of heterogeneously vancomycim-resistaut strain Mu3.

2005 ◽  
Vol 51 (3) ◽  
pp. 352-360 ◽  
Author(s):  
MARIA KPI ◽  
FUMIHIKO TAKEUCHI ◽  
KEIKO OKUMA ◽  
MAKOTO KURODA ◽  
LONGZHU CUI ◽  
...  
Keyword(s):  
Growth Rate ◽  
Cell Wall ◽  
Spontaneous Mutation ◽  
Vancomycin Resistance ◽  
Wall Thickening

scholarly journals Complete Reconstitution of the Vancomycin-Intermediate Staphylococcus aureus Phenotype of Strain Mu50 in Vancomycin-Susceptible S. aureus

2016 ◽  
Vol 60 (6) ◽  
pp. 3730-3742 ◽  
Author(s):  
Yuki Katayama ◽  
Miwa Sekine ◽  
Tomomi Hishinuma ◽  
Yoshifumi Aiba ◽  
Keiichi Hiramatsu
Keyword(s):  
Staphylococcus Aureus ◽  
Cell Wall ◽  
Mutant Strain ◽  
Vancomycin Resistance ◽  
Wall Thickening ◽  
Cell Physiology ◽  
Content Type ◽  
Sequence Deletion ◽  
Quadruple Mutant ◽  
Genetic Events

Complete reconstitution of the vancomycin-intermediateStaphylococcus aureus(VISA) phenotype of strain Mu50 was achieved by sequentially introducing mutations into six genes of vancomycin-susceptibleS. aureus(VSSA) strain N315ΔIP. The six mutated genes were detected in VISA strain Mu50 but not in N315ΔIP. Introduction of the mutation Ser329Leu intovraS, encoding the sensor histidine kinase of thevraSRtwo-component regulatory (TCR) system, and another mutation, Glu146Lys, intomsrR, belonging to the LytR-CpsA-Psr (LCP) family, increased the level of vancomycin resistance to that detected in heterogeneous vancomycin-intermediateS. aureus(hVISA) strain Mu3. Introduction of two more mutations, Asn197Ser intograRof thegraSRTCR system and His481Tyr intorpoB, encoding the β subunit of RNA polymerase, converted the hVISA strain into a VISA strain with the same level of vancomycin resistance as Mu50. Surprisingly, however, the constructed quadruple mutant strain ΔIP4 did not have a thickened cell wall, a cardinal feature of the VISA phenotype. Subsequent study showed that cell wall thickening was an inducible phenotype in the mutant strain, whereas it was a constitutive one in Mu50. Finally, introduction of the Ala297Val mutation intofdh2, which encodes a putative formate dehydrogenase, or a 67-amino-acid sequence deletion intosle1[sle1(Δ67aa)], encoding the hydrolase ofN-acetylmuramyl-l-alanine amidase in the peptidoglycan, converted inducible cell wall thickening into constitutive cell wall thickening.sle1(Δ67aa) was found to cause a drastic decrease in autolysis activity. Thus, all six mutated genes required for acquisition of the VISA phenotype were directly or indirectly involved in the regulation of cell physiology. The VISA phenotype seemed to be achieved through multiple genetic events accompanying drastic changes in cell physiology.

scholarly journals Correlation between Reduced Daptomycin Susceptibility and Vancomycin Resistance in Vancomycin-Intermediate Staphylococcus aureus

2006 ◽  
Vol 50 (3) ◽  
pp. 1079-1082 ◽  
Author(s):  
Longzhu Cui ◽  
Eiji Tominaga ◽  
Hui-min Neoh ◽  
Keiichi Hiramatsu
Keyword(s):  
Staphylococcus Aureus ◽  
Cell Wall ◽  
Vancomycin Resistance ◽  
Wall Thickening ◽  
Strong Positive Correlation ◽  
Physical Barrier ◽  
Positive Correlation

ABSTRACT We present here findings of a strong positive correlation between reduced daptomycin susceptibility and vancomycin resistance in vancomycin-intermediate Staphylococcus aureus (VISA). This correlation is related to cell wall thickening, suggesting that, similar to the case with vancomycin resistance in VISA, the physical barrier of a thickened cell wall may contribute to daptomycin resistance in S. aureus.

scholarly journals Cell Wall Thickening Is a Common Feature of Vancomycin Resistance in Staphylococcus aureus

2003 ◽  
Vol 41 (1) ◽  
pp. 5-14 ◽  
Author(s):  
L. Cui ◽  
X. Ma ◽  
K. Sato ◽  
K. Okuma ◽  
F. C. Tenover ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
Cell Wall ◽  
Vancomycin Resistance ◽  
Wall Thickening

scholarly journals In VivoStudies Suggest that Induction of VanS-Dependent Vancomycin Resistance Requires Binding of the Drug to d-Ala-d-Ala Termini in the Peptidoglycan Cell Wall

2013 ◽  
Vol 57 (9) ◽  
pp. 4470-4480 ◽  
Author(s):  
Min Jung Kwun ◽  
Gabriela Novotna ◽  
Andrew R. Hesketh ◽  
Lionel Hill ◽  
Hee-Jeon Hong
Keyword(s):  
Cell Wall ◽  
Transcriptional Activation ◽  
Streptomyces Coelicolor ◽  
Constitutive Expression ◽  
Transcriptional Response ◽  
Vancomycin Resistance ◽  
Content Type ◽  
Expression Of Genes ◽  
Peptidoglycan Cell Wall

ABSTRACTVanRS two-component regulatory systems are key elements required for the transcriptional activation of inducible vancomycin resistance genes in bacteria, but the precise nature of the ligand signal that activates these systems has remained undefined. Using the resistance system inStreptomyces coelicoloras a model, we have undertaken a series ofin vivostudies which indicate that the VanS sensor kinase in VanB-type resistance systems is activated by vancomycin in complex with thed-alanyl-d-alanine (d-Ala-d-Ala) termini of cell wall peptidoglycan (PG) precursors. Complementation of an essentiald-Ala-d-Ala ligase activity by constitutive expression ofvanAencoding a bifunctionald-Ala-d-Ala andd-alanyl-d-lactate (d-Ala-d-Lac) ligase activity allowed construction of strains that synthesized variable amounts of PG precursors containingd-Ala-d-Ala. Assays quantifying the expression of genes under VanRS control showed that the response to vancomycin in these strains correlated with the abundance ofd-Ala-d-Ala-containing PG precursors; strains producing a lower proportion of PG precursors terminating ind-Ala-d-Ala consistently exhibited a lower response to vancomycin. Pretreatment of wild-type cells with vancomycin or teicoplanin to saturate and mask thed-Ala-d-Ala binding sites in nascent PG also blocked the transcriptional response to subsequent vancomycin exposure, and desleucyl vancomycin, a vancomycin analogue incapable of interacting withd-Ala-d-Ala residues, failed to inducevangene expression. Activation of resistance by a vancomycin–d-Ala-d-Ala PG complex predicts a limit to the proportion of PG that can be derived from precursors terminating ind-Ala-d-Lac, a restriction also enforced by the bifunctional activity of the VanA ligase.

Cell wall thickening in two Ulva species in response to heavy metal marine pollution

2020 ◽  
Vol 35 ◽  
pp. 101125 ◽  
Author(s):  
Safia Zeroual ◽  
Salah Eddine El Bakkal ◽  
Mounir Mansori ◽  
Sabine Lhernould ◽  
Céline Faugeron-Girard ◽  
...  
Keyword(s):  
Heavy Metal ◽  
Cell Wall ◽  
Marine Pollution ◽  
Wall Thickening

Regulation of Cell Wall Thickening by a Medley of Mechanisms

2019 ◽  
Vol 24 (9) ◽  
pp. 853-866 ◽  
Author(s):  
Ian W. McCahill ◽  
Samuel P. Hazen
Keyword(s):  
Cell Wall ◽  
Wall Thickening

scholarly journals Increase in Cell Wall Thickening and Biomass Production by Overexpression of PmCesA2 in Poplar

2020 ◽  
Vol 11 ◽  
Author(s):  
Samaneh Sadat Maleki ◽  
Kourosh Mohammadi ◽  
Ali Movahedi ◽  
Fan Wu ◽  
Kong Shu Ji
Keyword(s):  
Cell Wall ◽  
Biomass Production ◽  
Wall Thickening

Stem Protective Tissue in Erythroxylum Tortuosum (Erythroxylaceae), A Fire Tolerant Species from Cerrado

IAWA Journal ◽  
2008 ◽  
Vol 29 (1) ◽  
pp. 69-77 ◽  
Author(s):  
Alexandre Antonio Alonso ◽  
Silvia Rodrigues Machado
Keyword(s):  
Cell Wall ◽  
Wall Thickening ◽  
Brazilian Cerrado ◽  
Tolerant Species ◽  
Phenolic Substances ◽  
Shrubby Species ◽  
Terminal Buds

The origin and structure are described of the secondary protective tissue in the stem of Erythorxylum tortuosum Mart., a fire tolerant shrubby species common in Brazilian cerrado. The highly tortuous stems are covered with thick bark which is more developed at the base of the stem. After fire in the cerrado, rhytidome fragments of the burned stem flake off, revealing newly formed cork. The first periderm appears near of the terminal buds and is iniated by periclinal divisions in subepidermal cells giving rise to radial rows of cells. The first phellogen is discernible only after the differentiation of the several radial rows of cork cells. Other phellogens have their origin in successively deeper layers of the cortex. The sucessive periderms are discontinuous around the circumference. The collapsed cells with phenolic substances and the accumulated dead cells cause the formation of discontinuous blackish lines, which delimit the sucessive periderms in the rhytidome. The rhytidome contains large quantities of sclereids developed from cell wall thickening of cortex cells. The occurrence of periderm in the young parts of the stem and of rhytidome in the older parts represents pyrophytic characteristics and may explain, in part, the fire tolerance of this species.

scholarly journals A Decrease in Mesophyll Conductance by Cell-Wall Thickening Contributes to Photosynthetic Downregulation

2020 ◽  
Vol 183 (4) ◽  
pp. 1600-1611 ◽  
Author(s):  
Daisuke Sugiura ◽  
Ichiro Terashima ◽  
John R. Evans
Keyword(s):  
Cell Wall ◽  
Wall Thickening ◽  
Mesophyll Conductance ◽  
Photosynthetic Downregulation
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