scholarly journals In vitro cell wall extensibility controls age-related changes in the growth rate of etiolated Arabidopsis hypocotyls

2015 ◽  
Vol 42 (11) ◽  
pp. 1068 ◽  
Author(s):  
Dmitry Suslov ◽  
Alexander Ivakov ◽  
Agnieszka K. Boron ◽  
Kris Vissenberg
Keyword(s):  
Growth Rate ◽  
Cell Wall ◽  
Creep Rate ◽  
Wall Stress ◽  
Cell Wall Extensibility ◽  
Age Related ◽  
Creep Measurements ◽  
Wall Extensibility

Plant cell growth is controlled by cell wall extensibility, which is currently estimated indirectly by various microtensile and nano/microindentation techniques. Their outputs differ in the accuracy of growth rate and in vivo extensibility prediction. Using the creep method we critically tested several metrics (creep rate, creep rate × stress–1, in vitro cell wall extensibility (ϕ) and in vitro cell wall yield threshold (y)) for their ability to predict growth rates of etiolated Arabidopsis thaliana (L. Heynh.) hypocotyls. We developed novel approaches for ϕ and y determination and statistical analysis based on creep measurements under single loads coupled with wall stress calculation. The best indicator of growth rate was ϕ because the 3-fold developmental decrease in the growth rate of 4- vs 3-day-old hypocotyls was accompanied by a 3-fold decrease in ϕ determined at pH 5. Although the acid-induced expansin-mediated creep of cell walls resulted exclusively from increasing ϕ values, the decrease in ϕ between 3- and 4-day-old hypocotyls was not mediated by a decrease in expansin abundance. We give practical recommendations on the most efficient use of creep rate, creep rate × stress–1, ϕ and y in different experimental situations and provide scripts for their automated calculations and statistical comparisons.

In-vivo measurement of cell-wall extensibility in maize coleoptiles: Effects of auxin and abscisic acid

Planta ◽  
1986 ◽  
Vol 169 (3) ◽  
pp. 437-442 ◽  
Author(s):  
U. Kutschera ◽  
P. Schopfer
Keyword(s):  
Cell Wall ◽  
Abscisic Acid ◽  
Cell Wall Extensibility ◽  
In Vivo Measurement ◽  
Wall Extensibility

scholarly journals Mutations inmmpLand in the Cell Wall Stress Stimulon Contribute to Resistance to Oxadiazole Antibiotics in Methicillin-Resistant Staphylococcus aureus

2014 ◽  
Vol 58 (10) ◽  
pp. 5841-5847 ◽  
Author(s):  
Qiaobin Xiao ◽  
Sergei Vakulenko ◽  
Mayland Chang ◽  
Shahriar Mobashery
Keyword(s):  
Staphylococcus Aureus ◽  
Cell Wall ◽  
Wall Stress ◽  
Methicillin Resistant ◽  
Content Type ◽  
Cell Wall Stress ◽  
A Cell ◽  
Putative Member

ABSTRACTStaphylococcus aureusis a leading cause of hospital- and community-acquired infections, which exhibit broad resistance to various antibiotics. We recently disclosed the discovery of the oxadiazole class of antibiotics, which hasin vitroandin vivoactivities against methicillin-resistantS. aureus(MRSA). We report herein that MmpL, a putative member of the resistance, nodulation, and cell division (RND) family of proteins, contributes to oxadiazole resistance in theS. aureusstrain COL. Through serial passages, we generated twoS. aureusCOL variants that showed diminished susceptibilities to an oxadiazole antibiotic. The MICs for the oxadiazole against one strain (designatedS. aureusCOLI) increased reproducibly 2-fold (to 4 μg/ml), while against the other strain (S. aureusCOLR), they increased >4-fold (to >8 μg/ml, the limit of solubility). The COLRstrain was derived from the COLIstrain. Whole-genome sequencing revealed 31 mutations inS. aureusCOLR, of which 29 were shared with COLI. Consistent with our previous finding that oxadiazole antibiotics inhibit cell wall biosynthesis, we found 13 mutations that occurred either in structural genes or in promoters of the genes of the cell wall stress stimulon. Two unique mutations inS. aureusCOLRwere substitutions in two genes that encode the putative thioredoxin (SACOL1794) and MmpL (SACOL2566). A role formmpLin resistance to oxadiazoles was discerned from gene deletion and complementation experiments. To our knowledge, this is the first report that a cell wall-acting antibiotic selects for mutations in the cell wall stress stimulon and the first to implicate MmpL in resistance to antibiotics inS. aureus.

scholarly journals Chitin Synthesis in a gas1 Mutant ofSaccharomyces cerevisiae

2000 ◽  
Vol 182 (17) ◽  
pp. 4752-4757 ◽  
Author(s):  
M-Henar Valdivieso ◽  
Laura Ferrario ◽  
Marina Vai ◽  
Angel Duran ◽  
Laura Popolo
Keyword(s):  
Cell Wall ◽  
Wall Stress ◽  
Chitinase Activity ◽  
Yeast Cells ◽  
Compensatory Mechanism ◽  
Chitin Synthesis ◽  
Regulatory Molecule ◽  
Defective Mutant

ABSTRACT The existence of a compensatory mechanism in response to cell wall damage has been proposed in yeast cells. The increase of chitin accumulation is part of this response. In order to study the mechanism of the stress-related chitin synthesis, we tested chitin synthase I (CSI), CSII, and CSIII in vitro activities in the cell-wall-defective mutant gas1Δ. CSI activity increased twofold with respect to the control, a finding in agreement with an increase in the expression of the CHS1 gene. However, deletion of theCHS1 gene did not affect the phenotype of thegas1Δ mutant and only slightly reduced the chitin content. Interestingly, in chs1 gas1 double mutants the lysed-bud phenotype, typical of chs1 null mutant, was suppressed, although in gas1 cells there was no reduction in chitinase activity. CHS3 expression was not affected in the gas1 mutant. Deletion of the CHS3 gene severely compromised the phenotype of gas1 cells, despite the fact that CSIII activity, assayed in membrane fractions, did not change. Furthermore, in chs3 gas1 cells the chitin level was about 10% that of gas1 cells. Thus, CSIII is the enzyme responsible for the hyperaccumulation of chitin in response to cell wall stress. However, the level of enzyme or the in vitro CSIII activity does not change. This result suggests that an interaction with a regulatory molecule or a posttranslational modification, which is not preserved during membrane fractionation, could be essential in vivo for the stress-induced synthesis of chitin.

scholarly journals Yapsins Are a Family of Aspartyl Proteases Required for Cell Wall Integrity in Saccharomyces cerevisiae

2005 ◽  
Vol 4 (8) ◽  
pp. 1364-1374 ◽  
Author(s):  
Damian J. Krysan ◽  
Elizabeth L. Ting ◽  
Claudia Abeijon ◽  
Lee Kroos ◽  
Robert S. Fuller
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Cell Wall ◽  
Specific Activity ◽  
Wall Stress ◽  
Cell Wall Integrity ◽  
Dependent Manner ◽  
Glucan Synthesis ◽  
Aspartyl Proteases

ABSTRACT The yeast cell wall is a crucial extracellular organelle that protects the cell from lysis during environmental stress and morphogenesis. Here, we demonstrate that the yapsin family of five glycosylphosphatidylinositol-linked aspartyl proteases is required for cell wall integrity in Saccharomyces cerevisiae. Yapsin null mutants show hypersensitivity to cell wall perturbation, and both the yps1Δ2Δ mutant and the quintuple yapsin mutant (5ypsΔ) undergo osmoremedial cell lysis at 37°C. The cell walls of both 5ypsΔ and yps1Δ2Δ mutants have decreased amounts of 1,3- and 1,6-β-glucan. Although there is decreased incorporation of both 1,3- and 1,6-β-glucan in the 5ypsΔ mutant in vivo, in vitro specific activity of both 1,3- and 1,6-β-glucan synthesis is similar to wild type, indicating that the yapsins affect processes downstream of glucan synthesis and that the yapsins may be involved in the incorporation or retention of cell wall glucan. Presumably as a response to the significant alterations in cell wall composition, the cell wall integrity mitogen-activated kinase signaling cascade (PKC1-MPK pathway) is basally active in 5ypsΔ. YPS1 expression is induced during cell wall stress and remodeling in a PKC1-MPK1-dependent manner, indicating that Yps1p is a direct, and important, output of the cell wall integrity response. The Candida albicans (SAP9) and Candida glabrata (CgYPS1) homologues of YPS1 complement the phenotypes of the yps1Δ mutant. Taken together, these data indicate that the yapsins play an important role in glucan homeostasis in S. cerevisiae and that yapsin homologues may play a similar role in the pathogenic yeasts C. albicans and C. glabrata.

In vitro and in vivo polysaccharides assembly: ultrastructural and cytochemical study of growing plant cell wall components.

1978 ◽  
Vol 36 (2) ◽  
pp. 434-435
Author(s):  
D. Reis ◽  
B. Vian ◽  
J. C. Roland
Keyword(s):  
Cell Wall ◽  
Self Assembly ◽  
Plant Cell Wall ◽  
Higher Plants ◽  
Three Dimensional ◽  
Cytochemical Study ◽  
Wall Components

Wall morphogenesis in higher plants is a problem still open to controversy. Until now the possibility of a transmembrane control and the involvement of microtubules were mostly envisaged. Self-assembly processes have been observed in the case of walls of Chlamydomonas and bacteria. Spontaneous gelling interactions between xanthan and galactomannan from Ceratonia have been analyzed very recently. The present work provides indications that some processes of spontaneous aggregation could occur in higher plants during the formation and expansion of cell wall.Observations were performed on hypocotyl of mung bean (Phaseolus aureus) for which growth characteristics and wall composition have been previously defined.In situ, the walls of actively growing cells (primary walls) show an ordered three-dimensional organization (fig. 1). The wall is typically polylamellate with multifibrillar layers alternately transverse and longitudinal. Between these layers intermediate strata exist in which the orientation of microfibrils progressively rotates. Thus a progressive change in the morphogenetic activity occurs.

Correlation between cell wall extensibility and the content of diferulic and ferulic acids in cell walls of Oryza sativa coleoptiles grown under water and in air

1991 ◽  
Vol 83 (3) ◽  
pp. 397-403 ◽  
Author(s):  
Kah-Siew Tan ◽  
Takayuki Hoson ◽  
Yoshio Masuda ◽  
Seiichiro Kamisaka
Keyword(s):  
Cell Wall ◽  
Oryza Sativa ◽  
Cell Walls ◽  
Cell Wall Extensibility ◽  
Ferulic Acids ◽  
Wall Extensibility

In vitro Cell Wall Stress Assay for Fusarium oxysporum

BIO-PROTOCOL ◽  
2016 ◽  
Vol 6 (17) ◽  
Author(s):  
Elena Pérez-Nadales ◽  
Antonio Di Pietro
Keyword(s):  
Cell Wall ◽  
Fusarium Oxysporum ◽  
Wall Stress ◽  
Cell Wall Stress

scholarly journals Regorafenib-Attenuated, Bleomycin-Induced Pulmonary Fibrosis by Inhibiting the TGF-β1 Signaling Pathway

2021 ◽  
Vol 22 (4) ◽  
pp. 1985
Author(s):  
Xiaohe Li ◽  
Ling Ma ◽  
Kai Huang ◽  
Yuli Wei ◽  
Shida Long ◽  
...  
Keyword(s):  
Pulmonary Fibrosis ◽  
Signaling Pathway ◽  
Transforming Growth Factor ◽  
Kinase Inhibitor ◽  
In Vivo Experiments ◽  
Age Related ◽  
And Migration ◽  
Tgf Β1

Idiopathic pulmonary fibrosis (IPF) is a fatal and age-related pulmonary disease. Nintedanib is a receptor tyrosine kinase inhibitor, and one of the only two listed drugs against IPF. Regorafenib is a novel, orally active, multi-kinase inhibitor that has similar targets to nintedanib and is applied to treat colorectal cancer and gastrointestinal stromal tumors in patients. In this study, we first identified that regorafenib could alleviate bleomycin-induced pulmonary fibrosis in mice. The in vivo experiments indicated that regorafenib suppresses collagen accumulation and myofibroblast activation. Further in vitro mechanism studies showed that regorafenib inhibits the activation and migration of myofibroblasts and extracellular matrix production, mainly through suppressing the transforming growth factor (TGF)-β1/Smad and non-Smad signaling pathways. In vitro studies have also indicated that regorafenib could augment autophagy in myofibroblasts by suppressing TGF-β1/mTOR (mechanistic target of rapamycin) signaling, and could promote apoptosis in myofibroblasts. In conclusion, regorafenib attenuates bleomycin-induced pulmonary fibrosis by suppressing the TGF-β1 signaling pathway.

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