Journal articles: 'Cell wall deficiency'

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Liao, Ya-Yun, Thomas J. Buckhout, and Wolfgang Schmidt. "Phosphate deficiency-induced cell wall remodeling." Plant Signaling & Behavior 6, no. 5 (May 2011): 700–702. http://dx.doi.org/10.4161/psb.6.5.15051.

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Wu, Weiwei, Shengnan Zhu, Qianqian Chen, Yan Lin, Jiang Tian, and Cuiyue Liang. "Cell Wall Proteins Play Critical Roles in Plant Adaptation to Phosphorus Deficiency." International Journal of Molecular Sciences 20, no. 21 (October 23, 2019): 5259. http://dx.doi.org/10.3390/ijms20215259.

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Phosphorus is one of the mineral nutrient elements essential for plant growth and development. Low phosphate (Pi) availability in soils adversely affects crop production. To cope with low P stress, remodeling of root morphology and architecture is generally observed in plants, which must be accompanied by root cell wall modifications. It has been documented that cell wall proteins (CWPs) play critical roles in shaping cell walls, transmitting signals, and protecting cells against environmental stresses. However, understanding of the functions of CWPs involved in plant adaptation to P deficiency remains fragmentary. The aim of this review was to summarize advances in identification and functional characterization of CWPs in responses to P deficiency, and to highlight the critical roles of CWPs in mediating root growth, P reutilization, and mobilization in plants.

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Ridge, S. C., J. B. Zabriskie, H. Osawa, T. Diamantstein, A. L. Oronsky, and S. S. Kerwar. "Administration of group A streptococcal cell walls to rats induces an interleukin 2 deficiency." Journal of Experimental Medicine 164, no. 1 (July 1, 1986): 327–32. http://dx.doi.org/10.1084/jem.164.1.327.

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Intraperitoneal administration of group A streptococcal cell walls to Lewis rats induces a chronic arthritis, whereas the Fischer strain is resistant to the development of the lesion. Spleen cells from cell wall-treated rats (Lewis and Fischer) are deficient in the synthesis of IL-2. Using an mAb directed against the rat IL-2-R, the present studies indicate that the expression of IL-2-R on spleens of cell wall-treated rats is normal. However, the addition of exogenous IL-2 to spleen cells cultured with Con A does not stimulate the mitogenic response.

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Vitković, Ljubiša. "Wall turnover deficiency of Bacillus subtilis Nil5 is due to a decrease in teichoic acid." Canadian Journal of Microbiology 33, no. 6 (June 1, 1987): 566–68. http://dx.doi.org/10.1139/m87-096.

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Bacillus subtilis Ni15 is deficient in cell wall turnover. This deficiency is removed if the medium contains 0.2 M NaCl, which does not affect growth. The levels of amidase and glucosaminidase, the most likely enzymes involved in turnover, were, in stationary phase Nil5 cells, similar to those in late-exponential phase cells of a standard strain. The Nil5 enzymes were not salt sensitive. However, the Nil5 walls contained 4.7-fold less phosphorus than the walls of the standard strain. Since the phosphorus content of B. subtilis walls reflects the level of teichoic acid, it is proposed that the turnover deficiency of this strain is due to a decrease in wall teichoic acid.

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Ongenae, Véronique, Ariane Briegel, and Dennis Claessen. "Cell wall deficiency as an escape mechanism from phage infection." Open Biology 11, no. 9 (September 2021): 210199. http://dx.doi.org/10.1098/rsob.210199.

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The cell wall plays a central role in protecting bacteria from some environmental stresses, but not against all. In fact, in some cases, an elaborate cell envelope may even render the cell more vulnerable. For example, it contains molecules or complexes that bacteriophages recognize as the first step of host invasion, such as proteins and sugars, or cell appendages such as pili or flagella. In order to counteract phages, bacteria have evolved multiple escape mechanisms, such as restriction-modification, abortive infection, CRISPR/Cas systems or phage inhibitors. In this perspective review, we present the hypothesis that bacteria may have additional means to escape phage attack. Some bacteria are known to be able to shed their cell wall in response to environmental stresses, yielding cells that transiently lack a cell wall. In this wall-less state, the bacteria may be temporarily protected against phages, since they lack the essential entities that are necessary for phage binding and infection. Given that cell wall deficiency can be triggered by clinically administered antibiotics, phage escape could be an unwanted consequence that limits the use of phage therapy for treating stubborn infections.

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Zhang, Cheng, Mingliang He, Zhexuan Jiang, Lan Liu, Junbao Pu, Wenjun Zhang, Sheliang Wang, and Fangsen Xu. "The Xyloglucan Endotransglucosylase/Hydrolase Gene XTH22/TCH4 Regulates Plant Growth by Disrupting the Cell Wall Homeostasis in Arabidopsis under Boron Deficiency." International Journal of Molecular Sciences 23, no. 3 (January 23, 2022): 1250. http://dx.doi.org/10.3390/ijms23031250.

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TCH4 is a xyloglucan endotransglucosylase/hydrolase (XTH) family member. Extensive studies have shown that XTHs are very important in cell wall homeostasis for plant growth and development. Boron (B), as an essential micronutrient for plants, plays an essential role in the cross-linking of cell wall pectin. However, the effect of B on cell wall organization is unclear. This study aimed to explore the mechanism of plant adaption to B stress by investigating the role of TCH4 in cell wall homeostasis. We conducted both plate and hydroponic cultures of wild-type Col-0 and overexpression and gene knockout lines of XTH22/TCH4 to analyze the phenotype, components, and characteristics of the cell wall using immunofluorescence, atomic force microscopy (AFM), and transmission electron microscopy (TEM). B deficiency induces the expression of TCH4. The overexpression lines of TCH4 presented more sensitivity to B deficiency than the wild-type Col-0, while the knockout lines of TCH4 were more resistant to low B stress. Up-regulation of TCH4 influenced the ratio of chelator-soluble pectin to alkali-soluble pectin and decreased the degree of methylesterification of pectin under B-deficient conditions. Moreover, we found that B deficiency disturbed the arrangement of cellulose, enlarged the gap between cellulose microfibrils, and decreased the mechanical strength of the cell wall, leading to the formation of a thickened and deformed triangular region of the cell wall. These symptoms were more profound in the TCH4 overexpression lines. Consistently, compared with Col-0, the O2− and MDA contents in the TCH4 overexpression lines increased under B-deficient conditions. This study identified the B-deficiency-induced TCH4 gene, which regulates cell wall homeostasis to influence plant growth under B-deficient conditions.

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Yin, Qi, Lu Kang, Yi Liu, Mirza Faisal Qaseem, Wenqi Qin, Tingting Liu, Huiling Li, Xiaomei Deng, and Ai-min Wu. "Boron deficiency disorders the cell wall in Neolamarckia cadamba." Industrial Crops and Products 176 (February 2022): 114332. http://dx.doi.org/10.1016/j.indcrop.2021.114332.

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Claessen, Dennis, and Jeff Errington. "Cell Wall Deficiency as a Coping Strategy for Stress." Trends in Microbiology 27, no. 12 (December 2019): 1025–33. http://dx.doi.org/10.1016/j.tim.2019.07.008.

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Gutierrez-Armijos, L. Roxana, Rodrigo A. C. Sussmann, Ariel M. Silber, Mauro Cortez, and Agustín Hernández. "Abnormal sterol-induced cell wall glucan deficiency in yeast is due to impaired glucan synthase transport to the plasma membrane." Biochemical Journal 477, no. 24 (December 18, 2020): 4729–44. http://dx.doi.org/10.1042/bcj20200663.

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Abnormal sterols disrupt cellular functions through yet unclear mechanisms. In Saccharomyces cerevisiae, accumulation of Δ8-sterols, the same type of sterols observed in patients of Conradi–Hünermann–Happle syndrome or in fungi after amine fungicide treatment, leads to cell wall weakness. We have studied the influence of Δ8-sterols on the activity of glucan synthase I, the protein synthetizing the main polymer in fungal cell walls, its regulation by the Cell Wall Integrity (CWI) pathway, and its transport from the endoplasmic reticulum to the plasma membrane. We ascertained that the catalytic characteristics were mostly unaffected by the presence of abnormal sterols but the enzyme was partially retained in the endoplasmic reticulum, leading to glucan deficit at the cell wall. Furthermore, we observed that glucan synthase I traveled through an unconventional exocytic route to the plasma membrane that is associated with low density intracellular membranes. Also, we found out that the CWI pathway remained inactive despite low glucan levels at the cell wall. Taken together, these data suggest that Δ8-sterols affect cell walls by inhibiting unconventional secretion of proteins leading to retention and degradation of glucan synthase I, while the compensatory CWI pathway is unable to activate. These results could be instrumental to understand defects of bone development in cholesterol biosynthesis disorders and fungicide mechanisms of action.

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Lam, Pui Ying, Lanxiang Wang, Andy C. W. Lui, Hongjia Liu, Yuri Takeda-Kimura, Mo-Xian Chen, Fu-Yuan Zhu, et al. "Deficiency in flavonoid biosynthesis genes CHS, CHI, and CHIL alters rice flavonoid and lignin profiles." Plant Physiology 188, no. 4 (December 28, 2021): 1993–2011. http://dx.doi.org/10.1093/plphys/kiab606.

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Abstract Lignin is a complex phenylpropanoid polymer deposited in the secondary cell walls of vascular plants. Unlike most gymnosperm and eudicot lignins that are generated via the polymerization of monolignols, grass lignins additionally incorporate the flavonoid tricin as a natural lignin monomer. The biosynthesis and functions of tricin-integrated lignin (tricin-lignin) in grass cell walls and its effects on the utility of grass biomass remain largely unknown. We herein report a comparative analysis of rice (Oryza sativa) mutants deficient in the early flavonoid biosynthetic genes encoding CHALCONE SYNTHASE (CHS), CHALCONE ISOMERASE (CHI), and CHI-LIKE (CHIL), with an emphasis on the analyses of disrupted tricin-lignin formation and the concurrent changes in lignin profiles and cell wall digestibility. All examined CHS-, CHI-, and CHIL-deficient rice mutants were largely depleted of extractable flavones, including tricin, and nearly devoid of tricin-lignin in the cell walls, supporting the crucial roles of CHS and CHI as committed enzymes and CHIL as a noncatalytic enhancer in the conserved biosynthetic pathway leading to flavone and tricin-lignin formation. In-depth cell wall structural analyses further indicated that lignin content and composition, including the monolignol-derived units, were differentially altered in the mutants. However, regardless of the extent of the lignin alterations, cell wall saccharification efficiencies of all tested rice mutants were similar to that of the wild-type controls. Together with earlier studies on other tricin-depleted grass mutant and transgenic plants, our results reflect the complexity in the metabolic consequences of tricin pathway perturbations and the relationships between lignin profiles and cell wall properties.

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Greenberg, M. L., and Q. Zhong. "Deficiency in mitochondrial anionic phospholipid synthesis impairs cell wall biogenesis." Biochemical Society Transactions 33, no. 5 (October 1, 2005): 1158. http://dx.doi.org/10.1042/bst20051158.

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Zhong, Q., and M. L. Greenberg. "Deficiency in mitochondrial anionic phospholipid synthesis impairs cell wall biogenesis." Biochemical Society Transactions 33, no. 5 (October 26, 2005): 1158–61. http://dx.doi.org/10.1042/bst0331158.

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Cardiolipin (CL) is the signature lipid of the mitochondrial membrane and plays a key role in mitochondrial physiology and cell viability. The importance of CL is underscored by the finding that the severe genetic disorder Barth syndrome results from defective CL composition and acylation. Disruption of PGS1, which encodes the enzyme that catalyses the committed step of CL synthesis, results in loss of the mitochondrial anionic phospholipids phosphatidylglycerol and CL. The pgs1Δ mutant exhibits severe growth defects at 37°C. To understand the essential functions of mitochondrial anionic lipids at elevated temperatures, we isolated suppressors of pgs1Δ that grew at 37°C. The present review summarizes our analysis of suppression of pgs1Δ growth defects by a mutant that has a loss-of-function mutation in KRE5, a gene involved in cell wall biogenesis.

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Kapopara, Piyushkumar, Johann von Felden, Oliver Soehnlein, Yong Wang, L. Christian Napp, Kristina Sonnenschein, Kai Wollert, et al. "Deficiency of MAPK-activated protein kinase 2 (MK2) prevents adverse remodelling and promotes endothelial healing after arterial injury." Thrombosis and Haemostasis 112, no. 12 (2014): 1264–76. http://dx.doi.org/10.1160/th14-02-0174.

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SummaryMaladaptive remodelling of the arterial wall after mechanical injury (e. g. angioplasty) is characterised by inflammation, neointima formation and media hypertrophy, resulting in narrowing of the affected artery. Moreover, mechanical injury of the arterial wall causes loss of the vessel protecting endothelial cell monolayer. Mitogen-activated protein kinase (MAPK)-activated protein kinase 2 (MK2), a major downstream target of p38 MAPK, regulates inflammation, cell migration and proliferation, essential processes for vascular remodelling and reendothelialisation. Therefore, we investigated the role of MK2 in remodelling and reendothelialisation after arterial injury in genetically modified mice in vivo. Hypercholesterolaemic low-densitylipoprotein- receptor-deficient mice (ldlr-/- ) were subjected to wire injury of the common carotid artery. MK2-deficiency (ldlr-/-/mk2-/- ) nearly completely prevented neointima formation, media hypertrophy, and lumen loss after injury. This was accompanied by reduced proliferation and migration of MK2-deficient smooth muscle cells. In addition, MK2-deficiency severely reduced monocyte adhesion to the arterial wall (day 3 after injury, intravital microscopy), which may be attributed to reduced expression of the chemokine ligands CCL2 and CCL5. In line, MK2-deficiency significantly reduced the content of monocytes, neutrophiles and lymphocytes of the arterial wall (day 7 after injury, flow cytometry). In conclusion, in a model of endothelial injury (electric injury), MK2-deficiency strongly increased proliferation of endothelial cells and improved reendothelialisation of the arterial wall after injury. Deficiency of MK2 prevents adverse remodelling and promotes endothelial healing of the arterial wall after injury, suggesting that MK2-inhibition is a very attractive intervention to prevent restenosis after percutaneous therapeutic angioplasty.

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Konno, Haruyoshi, Takako Nakato, and Kenji Katoh. "Characteristics, hydrolysis of cell wall polymers, and response to calcium deficiency of a cell wall-associated β-galactosidase from carrot cells." Journal of Plant Physiology 159, no. 1 (January 2002): 1–8. http://dx.doi.org/10.1078/0176-1617-00679.

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15

Liberini, Elisa, Sook-Ha Fan, Arnold S. Bayer, Christian Beck, Jacob Biboy, Patrice François, Joe Gray, et al. "Staphylococcus aureus Stress Response to Bicarbonate Depletion." International Journal of Molecular Sciences 25, no. 17 (August 26, 2024): 9251. http://dx.doi.org/10.3390/ijms25179251.

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Bicarbonate and CO2 are essential substrates for carboxylation reactions in bacterial central metabolism. In Staphylococcus aureus, the bicarbonate transporter, MpsABC (membrane potential-generating system) is the only carbon concentrating system. An mpsABC deletion mutant can hardly grow in ambient air. In this study, we investigated the changes that occur in S. aureus when it suffers from CO2/bicarbonate deficiency. Electron microscopy revealed that ΔmpsABC has a twofold thicker cell wall thickness compared to the parent strain. The mutant was also substantially inert to cell lysis induced by lysostaphin and the non-ionic surfactant Triton X-100. Mass spectrometry analysis of muropeptides revealed the incorporation of alanine into the pentaglycine interpeptide bridge, which explains the mutant’s lysostaphin resistance. Flow cytometry analysis of wall teichoic acid (WTA) glycosylation patterns revealed a significantly lower α-glycosylated and higher ß-glycosylated WTA, explaining the mutant’s increased resistance towards Triton X-100. Comparative transcriptome analysis showed altered gene expression profiles. Autolysin-encoding genes such as sceD, a lytic transglycosylase encoding gene, were upregulated, like in vancomycin-intermediate S. aureus mutants (VISA). Genes related to cell wall-anchored proteins, secreted proteins, transporters, and toxins were downregulated. Overall, we demonstrate that bicarbonate deficiency is a stress response that causes changes in cell wall composition and global gene expression resulting in increased resilience to cell wall lytic enzymes and detergents.

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Zhang, Hui, Ryu Watanabe, Gerald J. Berry, Augusto Vaglio, Yaping Joyce Liao, Kenneth J. Warrington, Jörg J. Goronzy, and Cornelia M. Weyand. "Immunoinhibitory checkpoint deficiency in medium and large vessel vasculitis." Proceedings of the National Academy of Sciences 114, no. 6 (January 23, 2017): E970—E979. http://dx.doi.org/10.1073/pnas.1616848114.

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Giant cell arteritis (GCA) causes autoimmune inflammation of the aorta and its large branches, resulting in aortic arch syndrome, blindness, and stroke. CD4+ T cells and macrophages form organized granulomatous lesions in the walls of affected arteries, destroy the tunica media, and induce ischemic organ damage through rapid intimal hyperplasia and luminal occlusion. Pathogenic mechanisms remain insufficiently understood; specifically, it is unknown whether the unopposed activation of the immune system is because of deficiency of immunoinhibitory checkpoints. Transcriptome analysis of GCA-affected temporal arteries revealed low expression of the coinhibitory ligand programmed death ligand-1 (PD-L1) concurrent with enrichment of the programmed death-1 (PD-1) receptor. Tissue-residing and ex vivo-generated dendritic cells (DC) from GCA patients were PD-L1lo, whereas the majority of vasculitic T cells expressed PD-1, suggesting inefficiency of the immunoprotective PD-1/PD-L1 immune checkpoint. DC–PD-L1 expression correlated inversely with clinical disease activity. In human artery-SCID chimeras, PD-1 blockade exacerbated vascular inflammation, enriched for PD-1+ effector T cells, and amplified tissue production of multiple T-cell effector cytokines, including IFN-γ, IL-17, and IL-21. Arteries infiltrated by PD-1+ effector T cells developed microvascular neoangiogenesis as well as hyperplasia of the intimal layer, implicating T cells in the maladaptive behavior of vessel wall endogenous cells. Thus, in GCA, a breakdown of the tissue-protective PD1/PD-L1 checkpoint unleashes vasculitic immunity and regulates the pathogenic remodeling of the inflamed arterial wall.

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Bélanger, G., and R. E. McQueen. "Leaf and stem nutritive value of timothy grown with varying N nutrition in spring and summer." Canadian Journal of Plant Science 79, no. 2 (April 1, 1999): 223–29. http://dx.doi.org/10.4141/p98-077.

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Nitrogen fertilization is known to have a limited effect on the digestibility of grasses. In a previous paper, however, we reported that N deficiency increased the proportion of leaves in the shoot biomass, and hence, indirectly increased the digestibility of timothy (Phleum pratense L). This was mitigated by the direct negative effect of N deficiency on the digestibility of leaves or stems or both early in the regrowth. The objective of this study was to determine the direct effect of N deficiency on three parameters of nutritive value of leaves and stems of timothy cv. Champ. The evolution of leaf and stem in vitro true digestibility (IVTD), in vitro cell wall digestibility (IVCWD), and neutral detergent fiber (NDF) concentration of field-grown timothy fertilized with four rates of N was studied during a spring and summer regrowth cycle by sampling at weekly intervals. The rate of decline in leaf nutritive value in spring was greater than that in summer, and was less than the rate of decline in stem nutritive value during spring. Nitrogen deficiency consistently increased the NDF concentration of leaves but had a lesser effect on the NDF concentration of stems. Nitrogen deficiency decreased leaf IVCWD when the leaf-to-weight ratio (LWR) was high early in the spring and summer regrowth cycles. At the end of regrowth when LWR values were low, leaf IVCWD was greatest when no N was applied. As a result, the negative effect of N deficiency on the leaf IVTD during the early part of the spring and summer regrowth cycles diminished as the regrowth cycles progressed. Nitrogen deficiency had a limited effect on stem IVCWD. We concluded that the direct negative effect of N deficiency on the digestibility of the timothy shoot biomass can be attributed primarily to its effect on the NDF concentration and cell wall digestibility of leaves. Key words: Phleum pratense L., grasses, digestibility, cell wall, nitrogen

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SULTANA, NIGHAT, HANNAH V. FLORANCE, ALEX JOHNS, and NICHOLAS SMIRNOFF. "Ascorbate deficiency influences the leaf cell wall glycoproteome in A rabidopsis thaliana." Plant, Cell & Environment 38, no. 2 (February 13, 2014): 375–84. http://dx.doi.org/10.1111/pce.12267.

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Yamamoto, Tsuyoshi, Atsuko Nakamura, Hiroaki Iwai, Tadashi Ishii, Jian Feng Ma, Ryusuke Yokoyama, Kazuhiko Nishitani, Shinobu Satoh, and Jun Furukawa. "Effect of silicon deficiency on secondary cell wall synthesis in rice leaf." Journal of Plant Research 125, no. 6 (April 13, 2012): 771–79. http://dx.doi.org/10.1007/s10265-012-0489-3.

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20

Findeklee, P., and H. E. Goldbach. "Rapid Effects of Boron Deficiency on Cell Wall Elasticity Modulus inCucurbita pepoRoots." Botanica Acta 109, no. 6 (December 1996): 463–65. http://dx.doi.org/10.1111/j.1438-8677.1996.tb00599.x.

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Markova, Nadya, Irina Haydoushka, Lilia Michailova, Rumyana Ivanova, Violeta Valcheva, Mimi Jourdanova, Tatyana Popova, and Tatyana Radoucheva. "Cell wall deficiency and its effect on methicillin heteroresistance in Staphylococcus aureus." International Journal of Antimicrobial Agents 31, no. 3 (March 2008): 255–60. http://dx.doi.org/10.1016/j.ijantimicag.2007.09.015.

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Wu, Xiuwen, Yanshu Hao, Muhammad Riaz, and Cuncang Jiang. "Changes in Leaf Structure and Chemical Compositions Investigated by FTIR Are Correlated with Different Low Potassium Adaptation of Two Cotton Genotypes." Agronomy 10, no. 4 (April 1, 2020): 479. http://dx.doi.org/10.3390/agronomy10040479.

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Potassium (K) is an essential macronutrient for plant growth and development. K deficiency seriously affects protein and carbohydrate synthesis in the leaves of plants. The present study was carried out with two cotton genotypes with low K tolerance to investigate the different changes on chemical composition and structure in leaves of K-efficient cotton genotypes under low K stress by using Fourier transform infrared spectroscopy (FTIR) technology. The results showed that K deficiency decreased the leaf photosynthetic pigments in both genotypes, but significant observations were noted in K-efficient genotype 103. FTIR spectra and semiquantitative analysis revealed that the cell membrane permeability, cell wall pectin, protein, and polysaccharides of leaves were greatly influenced by K deficiency, and the changes were more significant in the leaf of genotype 122, indicating a better adaptation to low K in genotype 103. The results of this study revealed that the difference of low K adaptation of these two cotton genotypes might be related to maintaining cell wall integrity and carbohydrate transport in cells. These different compositional and structural changes in the leaves of the two cotton genotypes under K-deficient level gain a new physiological mechanism of K efficiency in cotton.

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Schiffler, Bettina, Enrico Barth, Mamadou Daffé, and Roland Benz. "Corynebacterium diphtheriae: Identification and Characterization of a Channel-Forming Protein in the Cell Wall." Journal of Bacteriology 189, no. 21 (August 24, 2007): 7709–19. http://dx.doi.org/10.1128/jb.00864-07.

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ABSTRACT The cell wall fraction of the gram-positive, nontoxic Corynebacterium diphtheriae strain C8r(−) Tox− (= ATCC 11913) contained a channel-forming protein, as judged from reconstitution experiments with artificial lipid bilayer experiments. The channel-forming protein was present in detergent-treated cell walls and in extracts of whole cells obtained using organic solvents. The protein had an apparent molecular mass of about 66 kDa as determined on Tricine-containing sodium dodecyl sulfate-polyacrylamide gel electrophoresis gels and consisted of subunits having a molecular mass of about 5 kDa. Single-channel experiments with the purified protein suggested that the protein formed channels with a single-channel conductance of 2.25 nS in 1 M KCl. Further single-channel analysis suggested that the cell wall channel is wide and water filled because it has only slight selectivity for cations over anions and its conductance followed the mobility sequence of cations and anions in the aqueous phase. Antibodies raised against PorA, the subunit of the cell wall channel of Corynebacterium glutamicum, detected both monomers and oligomers of the isolated protein, suggesting that there are highly conserved epitopes in the cell wall channels of C. diphtheriae and PorA. Localization of the protein on the cell surface was confirmed by an enzyme-linked immunosorbent assay. The prospective homology of PorA with the cell wall channel of C. diphtheriae was used to identify the cell wall channel gene, cdporA, in the known genome of C. diphtheriae. The gene and its flanking regions were cloned and sequenced. CdporA is a protein that is 43 amino acids long and does not have a leader sequence. cdporA was expressed in a C. glutamicum strain that lacked the major outer membrane channels PorA and PorH. Organic solvent extracts of the transformed cells formed in lipid bilayer membranes the same channels as the purified CdporA protein of C. diphtheriae formed, suggesting that the expressed protein is able to complement the PorA and PorH deficiency of the C. glutamicum strain. The study is the first report of a cell wall channel in a pathogenic Corynebacterium strain.

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Liu, Hou Cheng, Wen Peng Liu, Shi Wei Song, Guang Wen Sun, and Ri Yuan Chen. "Effect of Calcium Nutrient on Calcium Distribution and Ultrastructure of Cell and Chloroplast in Bunching Onion Leaf." Applied Mechanics and Materials 142 (November 2011): 111–15. http://dx.doi.org/10.4028/www.scientific.net/amm.142.111.

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Effect of calcium nutrient on calcium distribution and ultrastructure of cell and chloroplast in Bunching Onion (Allium fistulosum L. var. caespitosum Makino) leaf was studied in sands with 4 Ca2+ treatments (0, 40, 80 and 160 mg/L ), in which the solution was Hoagland's. Localization and distribution of calcSuperscript textium and the influence of calcium nutrition on cell ultrastructure were observed by transmission electron microscopy combined with in situ precipitation of calcium with potassium pyroantimonate technique. The results showed that Ca2+ were mainly located in cell membrane, vacuoles, envelope of chloroplast and intercellular space in normal cells of bunching onion, however, Ca2+ was found to compartment in cytosol in large quantity, and the release of membrane-associated Ca2+ to cytosol and wall-associated Ca2+ to the intercellular spaces was observed in Ca-deficient leaves. In serious Ca-deficient leaves, Ca2+ quantities in cell decreased. Under Ca-deficiency, chloroplast membranes, plasma membranes and nuclear membranes were damaged, and cell walls disassociated, an enlarged space could be found between cells. In serious Ca-deficient leaves, cell compartmentation was destroyed, chloroplast deformed, plasma separated from cell wall, then whole cell constricted.

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Tiwari, Kiran B., Craig Gatto, Suzanne Walker, and Brian J. Wilkinson. "Exposure ofStaphylococcus aureusto Targocil Blocks Translocation of the Major Autolysin Atl across the Membrane, Resulting in a Significant Decrease in Autolysis." Antimicrobial Agents and Chemotherapy 62, no. 7 (May 7, 2018): e00323-18. http://dx.doi.org/10.1128/aac.00323-18.

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ABSTRACTPeptidoglycan (PG) and wall teichoic acid (WTA) are the major staphylococcal cell wall components, and WTA biosynthesis has recently been explored for drug development. Targocil is a novel agent that targets the TarG subunit of the WTA translocase (TarGH) that transports WTA across the membrane to the wall. Previously we showed that targocil treatment of a methicillin-susceptibleStaphylococcus aureusstrain led to a rapid shut down of cellular autolysis. Targocil II, which targets the TarH subunit of TarGH, also resulted in a drastic decrease in autolysis. Here, we address the mechanism of targocil-mediated decreased autolysis. The mechanism is WTA dependent since targocil treatment decreased autolysis in methicillin-resistant strains but not in a WTA-deficient mutant. Similar to cellular autolysis, autolysin-retaining crude cell walls isolated from targocil-treated cells had vastly decreased autolytic activity compared to those from untreated cells. Purified cell walls from control and targocil-treated cells, which lack autolytic activity, were similarly susceptible to lysozyme and lysostaphin and had similar O-acetyl contents, indicating that targocil treatment did not grossly alter PG structure and chemistry. Purified cell walls from targocil-treated cells were highly susceptible to autolysin extracts, supporting the notion that targocil treatment led to decreased autolysin in the crude cell walls. Quantitative real-time PCR analysis revealed that the decrease in autolysis in the targocil-exposed cells was not due to transcriptional repression of the autolysin genesatl,lytM,lytN, andsle1. Zymographic analysis of peptidoglycan hydrolase profiles showed a deficiency of cell surface autolysins in targocil-treated cells but higher activity in cell membrane fractions. Here, we propose that the untranslocated WTA molecules in the targocil-exposed cells sequester Atl at the membrane, resulting in significantly decreased autolysis.

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Tu, Bin, Tao Zhang, Yuping Wang, Li Hu, Jin Li, Ling Zheng, Yi Zhou, et al. "Membrane-associated xylanase-like protein OsXYN1 is required for normal cell wall deposition and plant development in rice." Journal of Experimental Botany 71, no. 16 (April 27, 2020): 4797–811. http://dx.doi.org/10.1093/jxb/eraa200.

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Abstract The rice (Oryza sativa) genome encodes 37 putative β-1,4-xylanase proteins, but none of them has been characterized at the genetic level. In this work, we report the isolation of slim stem (ss) mutants with pleiotropic defects, including dwarfism, leaf tip necrosis, and withered and rolled leaves under strong sunlight. Map-based cloning of the ss1 mutant identified the candidate gene as OsXyn1 (LOC_03g47010), which encodes a xylanase-like protein belonging to the glycoside hydrolase 10 (GH10) family. OsXyn1 was found to be widely expressed, especially in young tissues. Subcellular localization analysis showed that OsXyn1 encodes a membrane-associated protein. Physiological analysis of ss1 and the allelic ss2 mutant revealed that water uptake was partially compromised in these mutants. Consistently, the plant cell wall of the mutants exhibited middle lamella abnormalities or deficiencies. Immunogold assays revealed an unconfined distribution of xylan in the mutant cell walls, which may have contributed to a slower rate of plant cell wall biosynthesis and delayed plant growth. Additionally, water deficiency caused abscisic acid accumulation and triggered drought responses in the mutants. The findings that OsXyn1 is involved in plant cell wall deposition and the regulation of plant growth and development help to shed light on the functions of the rice GH10 family.

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Meidani, Christianna, Nikoletta G. Ntalli, Eleni Giannoutsou, and Ioannis-Dimosthenis S. Adamakis. "Cell Wall Modifications in Giant Cells Induced by the Plant Parasitic Nematode Meloidogyne incognita in Wild-Type (Col-0) and the fra2 Arabidopsis thaliana Katanin Mutant." International Journal of Molecular Sciences 20, no. 21 (November 2, 2019): 5465. http://dx.doi.org/10.3390/ijms20215465.

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Meloidogyne incognita is a root knot nematode (RKN) species which is among the most notoriously unmanageable crop pests with a wide host range. It inhabits plants and induces unique feeding site structures within host roots, known as giant cells (GCs). The cell walls of the GCs undergo the process of both thickening and loosening to allow expansion and finally support nutrient uptake by the nematode. In this study, a comparative in situ analysis of cell wall polysaccharides in the GCs of wild-type Col-0 and the microtubule-defective fra2 katanin mutant, both infected with M. incognita has been carried out. The fra2 mutant had an increased infection rate. Moreover, fra2 roots exhibited a differential pectin and hemicellulose distribution when compared to Col-0 probably mirroring the fra2 root developmental defects. Features of fra2 GC walls include the presence of high-esterified pectic homogalacturonan and pectic arabinan, possibly to compensate for the reduced levels of callose, which was omnipresent in GCs of Col-0. Katanin severing of microtubules seems important in plant defense against M. incognita, with the nematode, however, to be nonchalant about this “katanin deficiency” and eventually induce the necessary GC cell wall modifications to establish a feeding site.

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İşkil, Rabia, and Yonca Surgun-Acar. "The effect of 24-epibrassinolide on gene expression related to cell walls under boron deficiency and toxicity in the leaves of Arabidopsis thaliana." Botanica Serbica 46, no. 1 (2022): 7–15. http://dx.doi.org/10.2298/botserb2201007i.

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The changing composition of plant cell walls allows for the continuation of the existing structure under normal conditions and also the protection of physical integrity under altering environmental conditions. In this study, the possible effects of the 24-Epibrassinolide (EBL) hormone under boron (B) deficiency and toxicity conditions on the expression of cell wall-related genes [cellulose synthase (CESA), expansin (EXP), xyloglucan endotransglucosylase/hydrolase (XTH) and pectin methylesterase (PME)] were investigated in the rosette leaves of Arabidopsis thaliana. For this purpose, 0 or 3000 ?M of boric acid (BA) and/or 1 ?M of EBL were applied to the plants which were grown in a hydroponic medium for five and ten weeks. While B-toxicity elevated the mRNA levels of the CESA4 and CESA8 genes in the leaves of the five-week-old plants, B-stress (B-deficiency and -toxicity) caused an increase in the expression of the CESA4, CESA6, and CESA8 genes in the ten-week-old plants. The transcript levels of the EXPA5 gene increased under B-stress in the ten-week-old plants whereas the expression of the EXPA8 gene decreased when compared to the control at two developmental stages. Co-treatment of EBL and B-stress strongly elevated the transcript level of the EXPA5 gene in the ten-week-old plants and the EXPA8 gene at both developmental stages. The EXPA14 and XTH23 genes exhibited distinct expression profiles under B-deficiency and -toxicity in both the five- and ten-week-old plants. The transcript level of the XTH21 gene was upregulated in the leaves of the plants exposed to B-stress. The mRNA level of the PME2 and PME41 genes was generally upregulated in response to B-stress in both the five- and ten-week-old plants. 24-Epibrassinolide alone and in combination with B-stress led to a remarkable increase in the expression of the XTH and PME genes compared to the control. These results demonstrate that cell wall genes generally show a similar pattern of expression at both developmental stages and the EBL hormone induces changes in the expression levels of cell wall-related genes under B-stress.

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Zhao, Heng, Daniel M. Roistacher, and John D. Helmann. "Aspartate deficiency limits peptidoglycan synthesis and sensitizes cells to antibiotics targeting cell wall synthesis inBacillus subtilis." Molecular Microbiology 109, no. 6 (August 20, 2018): 826–44. http://dx.doi.org/10.1111/mmi.14078.

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Ozgen, Senay, James S. Busse, and Jiwan P. Palta. "Influence of Root Zone Calcium on Shoot Tip Necrosis and Apical Dominance of Potato Shoot: Simulation of This Disorder by Ethylene Glycol Tetra Acetic Acid and Prevention by Strontium." HortScience 46, no. 10 (October 2011): 1358–62. http://dx.doi.org/10.21273/hortsci.46.10.1358.

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The important roles of calcium on plant growth and development including cell division and cell elongation is well documented. The purpose of the present study was to determine the impact of root zone calcium on the growth and health of potato apical meristem and on the maintenance of apical dominance. For this purpose, single-node potato cuttings (Solanum tuberosum L. cv. Dark Red Norland) were grown in sterilized modified Murashige and Skoog (MS) media containing varying concentrations of calcium (1 to 3000 μM). After 13 to 30 d of growth, plantlets were harvested and data for height of the main shoot and for the number of axillary shoots produced were recorded. Plantlets were ashed and tissue calcium concentration was determined. Shoot height was retarded with decreasing concentration of calcium in the media. Calcium deficiency induced shoot tip injury and loss of apical dominance. Tip injury was followed by the development of axillary shoots. The number of axillary shoots increased from one to 21 as calcium concentration in the media decreased from 3000 to 1 μM. At calcium concentration of 1500 μM or higher, there was a single main shoot with no axillary shoots. Addition of ethylene glycol tetra acetic acid (EGTA), a calcium chelator, to the media with 2720 μM calcium (sufficient calcium) resulted in the development of shoot injury and in the formation of axillary shoots. Calcium deficiency injury symptoms were prevented by the addition of a calcium analog, strontium, to MS media deficient in calcium. Strontium has been reported to strongly bind to plant cell walls and the inclusion of strontium prevented injury in shoots of plants grown on calcium-deficient media. These results suggest that strontium is able to mimic the role of calcium in the maintenance of cell wall integrity and supports previous studies that showed that calcium deficiency results from cell wall collapse of the subapical cells.

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Lin, Lijin, Zhiyu Li, Caifang Wu, Yaxin Xu, Jin Wang, Xiulan Lv, Hui Xia, Dong Liang, Zhi Huang, and Yi Tang. "Melatonin Promotes Iron Reactivation and Reutilization in Peach Plants under Iron Deficiency." International Journal of Molecular Sciences 24, no. 22 (November 9, 2023): 16133. http://dx.doi.org/10.3390/ijms242216133.

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The yellowing of leaves due to iron deficiency is a prevalent issue in peach production. Although the capacity of exogenous melatonin (MT) to promote iron uptake in peach plants has been demonstrated, its underlying mechanism remains ambiguous. This investigation was carried out to further study the effects of exogenous MT on the iron absorption and transport mechanisms of peach (Prunus persica) plants under iron-deficient conditions through transcriptome sequencing. Under both iron-deficient and iron-supplied conditions, MT increased the content of photosynthetic pigments in peach leaves and decreased the concentrations of pectin, hemicellulose, cell wall iron, pectin iron, and hemicellulose iron in peach plants to a certain extent. These effects stemmed from the inhibitory effect of MT on the polygalacturonase (PG), cellulase (Cx), phenylalanine ammonia-lyase (PAL), and cinnamoyl-coenzyme A reductase (CCR) activities, as well as the promotional effect of MT on the cinnamic acid-4-hydroxylase (C4H) activity, facilitating the reactivation of cell wall component iron. Additionally, MT increased the ferric-chelate reductase (FCR) activity and the contents of total and active iron in various organs of peach plants under iron-deficient and iron-supplied conditions. Transcriptome analysis revealed that the differentially expressed genes (DEGs) linked to iron metabolism in MT-treated peach plants were primarily enriched in the aminoacyl-tRNA biosynthesis pathway under iron-deficient conditions. Furthermore, MT influenced the expression levels of these DEGs, regulating cell wall metabolism, lignin metabolism, and iron translocation within peach plants. Overall, the application of exogenous MT promotes the reactivation and reutilization of iron in peach plants.

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Bolaños, Luis, Isidro Abreu, Ildefonso Bonilla, Juan J. Camacho-Cristóbal, and María Reguera. "What Can Boron Deficiency Symptoms Tell Us about Its Function and Regulation?" Plants 12, no. 4 (February 9, 2023): 777. http://dx.doi.org/10.3390/plants12040777.

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On the eve of the 100th anniversary of Dr. Warington’s discovery of boron (B) as a nutrient essential for higher plants, “boronists” have struggled to demonstrate a role beyond its structural function in cell walls dimerizing pectin molecules of rhamnogalacturonan II (RGII). In this regard, B deficiency has been associated with a plethora of symptoms in plants that include macroscopic symptoms like growth arrest and cell death and biochemical or molecular symptoms that include changes in cell wall pore size, apoplast acidification, or a steep ROS production that leads to an oxidative burst. Aiming to shed light on B functions in plant biology, we proposed here a unifying model integrating the current knowledge about B function(s) in plants to explain why B deficiency can cause such remarkable effects on plant growth and development, impacting crop productivity. In addition, based on recent experimental evidence that suggests the existence of different B ligands other than RGII in plant cells, namely glycolipids, and glycoproteins, we proposed an experimental pipeline to identify putative missing ligands and to determine how they would integrate into the above-mentioned model.

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Yokoyama, Chieko, Manabu Shimonishi, Toshihisa Hatae, Tomoko Yabuki, Susumu Ohkawara, Masayuki Wada, Tatemi Todaka, Hiroji Yanamoto, Jyunji Takeda, and Tadashi Tanabe. "Effects on the vascular wall of overexpression and deficiency of prostacyclin synthase." Prostaglandins & Other Lipid Mediators 59, no. 1-6 (December 1999): 111. http://dx.doi.org/10.1016/s0090-6980(99)90346-5.

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Zakharova, Irina N., Irina V. Berezhnaya, and Aleksandra I. Sgibneva. "Choline deficiency in the body, clinical manifestations and long-term consequences." Pediatrics. Consilium Medicum, no. 1 (May 10, 2022): 66–71. http://dx.doi.org/10.26442/26586630.2022.1.201510.

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Choline, a substance essential for the existence of any organism, is the basis for the synthesis of phosphatidylcholine and sphingomyelin, the two main phospholipids of cell membranes. Acetylcholine is the main neurotransmitter of the parasympathetic nervous system, i.e. part of the autonomic nervous system. It affects smooth muscles, vascular wall tone, heart rate and regulates metabolism as a source of methyl groups. Choline enters the body through food and is partially synthesized endogenously. Choline plays an important role in gene expression, cell membrane signalling, lipid transport and metabolism, and early infant brain development. Choline deficiency increases the risk of cardiovascular and metabolic disorders. Current scientific evidence suggests a negative effect of choline deficiency on the development of non-alcoholic fatty liver disease. Choline deficiency is associated with impaired memory, concentration, and cognitive functions. This article deals with the mechanisms of choline influence on the organism and possibility of choline deficiency correction in the organism.

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Matthes, Michaela S., Janlo M. Robil, and Paula McSteen. "From element to development: the power of the essential micronutrient boron to shape morphological processes in plants." Journal of Experimental Botany 71, no. 5 (January 27, 2020): 1681–93. http://dx.doi.org/10.1093/jxb/eraa042.

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Abstract Deficiency of the essential nutrient boron (B) in the soil is one of the most widespread micronutrient deficiencies worldwide, leading to developmental defects in root and shoot tissues of plants, and severe yield reductions in many crops. Despite this agricultural importance, the underlying mechanisms of how B shapes plant developmental and morphological processes are still not unequivocally understood in detail. This review evaluates experimental approaches that address our current understanding of how B influences plant morphological processes by focusing on developmental defects observed under B deficiency. We assess what is known about mechanisms that control B homeostasis and specifically highlight: (i) limitations in the methodology that is used to induce B deficiency; (ii) differences between mutant phenotypes and normal plants grown under B deficiency; and (iii) recent research on analyzing interactions between B and phytohormones. Our analysis highlights the need for standardized methodology to evaluate the roles of B in the cell wall versus other parts of the cell.

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Missiou, Anna, Philipp Rudolf, Peter Stachon, Dennis Wolf, Nerea Varo, Peter Aichele, Christian Colberg, et al. "TRAF5 Deficiency Accelerates Atherogenesis in Mice by Increasing Inflammatory Cell Recruitment and Foam Cell Formation." Circulation Research 107, no. 6 (September 17, 2010): 757–66. http://dx.doi.org/10.1161/circresaha.110.219295.

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Rationale: Tumor necrosis factor receptor–associated factors (TRAFs) are cytoplasmic adaptor proteins for the TNF/interleukin-1/Toll-like receptor superfamily. Ligands of this family comprise multiple important cytokines such as TNFα, CD40L, and interleukin-1β that promote chronic inflammatory diseases such as atherosclerosis. We recently reported overexpression of TRAF5 in murine and human atheromata and that TRAF5 promotes inflammatory functions of cultured endothelial cells and macrophages. Objective: This study tested the hypothesis that TRAF5 modulates atherogenesis in vivo. Methods and Results: Surprisingly, TRAF5 −/− /LDLR −/− mice consuming a high-cholesterol diet for 18 weeks developed significantly larger atherosclerotic lesions than did TRAF5 +/+ /LDLR −/− controls. Plaques of TRAF5-deficient animals contained more lipids and macrophages, whereas smooth muscle cells and collagen remained unchanged. Deficiency of TRAF5 in endothelial cells or in leukocytes enhanced adhesion of inflammatory cells to the endothelium in dynamic adhesion assays in vitro and in murine vessels imaged by intravital microscopy in vivo. TRAF5 deficiency also increased expression of adhesion molecules and chemokines and potentiated macrophage lipid uptake and foam cell formation. These findings coincided with increased activation of JNK and appeared to be independent of TRAF2. Finally, patients with stable or acute coronary heart disease had significantly lower amounts of TRAF5 mRNA in blood compared with healthy controls. Conclusions: Unexpectedly, TRAF5 deficiency accelerates atherogenesis in mice, an effect likely mediated by increased inflammatory cell recruitment to the vessel wall and enhanced foam cell formation.

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Tao, Ye, Jing Huang, Huai Kang Jing, Ren Fang Shen, and Xiao Fang Zhu. "Jasmonic acid is involved in root cell wall phosphorus remobilization through the nitric oxide dependent pathway in rice." Journal of Experimental Botany 73, no. 8 (January 27, 2022): 2618–30. http://dx.doi.org/10.1093/jxb/erac023.

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Abstract Jasmonic acid (JA) is involved in phosphorus (P) stress in plants, but its underlying molecular mechanisms are still elusive. In this study, we found root endogenous JA content in rice increased under P deficiency (-P), suggesting that JA might participate in P homeostasis in plants. This hypothesis was further confirmed through the addition of exogenous JA (+JA), as this could increase both the root and shoot soluble P content through regulating root cell wall P reutilization. In addition, –P+JA treatment significantly induced the expression of P transporter gene OsPT2, together with increased xylem P content, implying that JA is also important for P translocation from the root to the shoot in P-deficient rice. Furthermore, the accumulation of the molecular signal nitric oxide (NO) was enhanced under –P+JA treatment when compared with –P treatment alone, while the addition of c-PTIO, a scavenger of NO, could reverse the P-deficient phenotype alleviated by JA. Taken together, our results reveal a JA-NO-cell wall P reutilization pathway under P deficiency in rice.

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Bizzini, Alain, Paul Majcherczyk, Siham Beggah-Möller, Blazenka Soldo, José M. Entenza, Muriel Gaillard, Philippe Moreillon, and Vladimir Lazarevic. "Effects of α-phosphoglucomutase deficiency on cell wall properties and fitness in Streptococcus gordonii." Microbiology 153, no. 2 (February 1, 2007): 490–98. http://dx.doi.org/10.1099/mic.0.29256-0.

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Zhu, Xiao Fang, Gui Jie Lei, Tao Jiang, Yu Liu, Gui Xin Li, and Shao Jian Zheng. "Cell wall polysaccharides are involved in P-deficiency-induced Cd exclusion in Arabidopsis thaliana." Planta 236, no. 4 (April 25, 2012): 989–97. http://dx.doi.org/10.1007/s00425-012-1652-8.

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Sziva, Réka Eszter, Zoltán Fontányi, Éva Pál, Leila Hadjadj, Anna Monori-Kiss, Eszter Mária Horváth, Rita Benkő, et al. "Vitamin D Deficiency Induces Elevated Oxidative and Biomechanical Damage in Coronary Arterioles in Male Rats." Antioxidants 9, no. 10 (October 15, 2020): 997. http://dx.doi.org/10.3390/antiox9100997.

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Background: Several reports prove interconnection between vitamin D (VD) deficiency and increased cardiovascular risk. Our aim was to investigate the effects of VD status on biomechanical and oxidative–nitrative (O–N) stress parameters of coronary arterioles in rats. Methods: 4-week-old male Wistar rats were divided into a control group (11 animals) with optimal VD supply (300 IU/kgbw/day) and a VD-deficient group (11 animals, <5 IU/kg/day). After 8 weeks, coronary arteriole segments were prepared. Geometrical, elastic, and biomechanical characteristics were measured by in vitro arteriography. O–N stress markers were investigated by immunohistochemistry. Results: Inner radius decreased; wall thickness and wall-thickness/lumen diameter ratio increased; tangential wall stress and elastic modulus were reduced in VD-deficient group. No difference could be found in wall-cross-sectional area, intima-media area %. While the elastic elements of the vessel wall decreased, the α-smooth muscle actin (α-SMA) immunostaining intensity showed no changes. Significant elevation was found in the lipid peroxidation marker of 4-hidroxy-2-nonenal (HNE), while other O–N stress markers staining intensity (poly(ADP)ribose, 3-nitrotyrosine) did not change. Conclusions: Inward eutrophic remodeling has developed. The potential background of these impairments may involve the initial change in oxidative damage markers (HNE). These mechanisms can contribute to the increased incidence of the cardiovascular diseases in VD deficiency.

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García-Hernández, Edith del R., and Gladys I. Cassab López. "Structural cell wall proteins from five pollen species and their relationship with boron." Brazilian Journal of Plant Physiology 17, no. 4 (December 2005): 375–81. http://dx.doi.org/10.1590/s1677-04202005000400005.

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Boron (B) is an essential micronutrient for the survival of vascular plants. The most severe effect derived from a deficiency of B is the alteration of cell wall biogenesis and pollen germination. We investigated pollen of plant species that require B for germination (Zea may L. and Nicotiana tabacum L.), as well as those that can germinate without B (Pinus sp, Lilum longiflorum, Impatiens sp.). In both groups, B addition in the growth medium increased the length of the pollen tube after germination. Hydroxyproline Rich Glycoproteins (HRGPs) are the most abundant cell wall structural proteins of dicotyledonous plants and the sexual tissues of monocotyledonous plants. Here, we show that maize pollen accumulated a significant pool of hydroxyproline (Hyp) and 63% of this amino acid was localized in the pollen tube wall. Maize pollen germinated in the presence of B accumulated soluble (48%) and non-soluble (16%) Hyp in the pollen tube wall in contrast to maize pollen germinated without B. In addition, B seems to modify the amount of HRGPs that become cross-linked to the wall. Immunolocalization of HRGPs showed that these glycoproteins were preferentially localized in the pollen tube of maize, not in the pollen grain itself. Hence, B might affect the assembling of HRGPs in the wall of pollen tubes grown in vitro.

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Kohorn, Bruce D., Bridgid E. Greed, Gregory Mouille, Stéphane Verger, and Susan L. Kohorn. "Effects of Arabidopsis wall associated kinase mutations on ESMERALDA1 and elicitor induced ROS." PLOS ONE 16, no. 5 (May 20, 2021): e0251922. http://dx.doi.org/10.1371/journal.pone.0251922.

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Angiosperm cell adhesion is dependent on interactions between pectin polysaccharides which make up a significant portion of the plant cell wall. Cell adhesion in Arabidopsis may also be regulated through a pectin-related signaling cascade mediated by a putative O-fucosyltransferase ESMERALDA1 (ESMD1), and the Epidermal Growth Factor (EGF) domains of the pectin binding Wall associated Kinases (WAKs) are a primary candidate substrate for ESMD1 activity. Genetic interactions between WAKs and ESMD1 were examined using a dominant hyperactive allele of WAK2, WAK2cTAP, and a mutant of the putative O-fucosyltransferase ESMD1. WAK2cTAP expression results in a dwarf phenotype and activation of the stress response and reactive oxygen species (ROS) production, while esmd1 is a suppressor of a pectin deficiency induced loss of adhesion. Here we find that esmd1 suppresses the WAK2cTAP dwarf and stress response phenotype, including ROS accumulation and gene expression. Additional analysis suggests that mutations of the potential WAK EGF O-fucosylation site also abate the WAK2cTAP phenotype, yet only evidence for an N-linked but not O-linked sugar addition can be found. Moreover, a WAK locus deletion allele has no effect on the ability of esmd1 to suppress an adhesion deficiency, indicating WAKs and their modification are not a required component of the potential ESMD1 signaling mechanism involved in the control of cell adhesion. The WAK locus deletion does however affect the induction of ROS but not the transcriptional response induced by the elicitors Flagellin, Chitin and oligogalacturonides (OGs).

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Nonaka, Risa, Takafumi Iesaki, Aurelien Kerever, and Eri Arikawa-Hirasawa. "Increased Risk of Aortic Dissection with Perlecan Deficiency." International Journal of Molecular Sciences 23, no. 1 (December 28, 2021): 315. http://dx.doi.org/10.3390/ijms23010315.

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Perlecan (HSPG2), a basement membrane-type heparan sulfate proteoglycan, has been implicated in the development of aortic tissue. However, its role in the development and maintenance of the aortic wall remains unknown. Perlecan-deficient mice (Hspg2−/−-Tg: Perl KO) have been found to show a high frequency (15–35%) of aortic dissection (AD). Herein, an analysis of the aortic wall of Perl KO mice revealed that perlecan deficiency caused thinner and partially torn elastic lamina. Compared to the control aortic tissue, perlecan-deficient aortic tissue showed a significant decrease in desmosine content and an increase in soluble tropoelastin levels, implying the presence of immature elastic fibers in Perl KO mice. Furthermore, the reduced expression of the smooth muscle cell contractile proteins actin and myosin in perlecan-deficient aortic tissue may explain the risk of AD. This study showed that a deficiency in perlecan, which is localized along the elastic lamina and at the interface between elastin and fibrillin-1, increased the risk of AD, largely due to the immaturity of extracellular matrix in the aortic tissue. Overall, we proposed a new model of AD that considers the deficiency of extracellular molecule perlecan as a risk factor.

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Wu, Peipei, Mingsheng Peng, Zhigang Li, Ning Yuan, Qian Hu, Cliff E. Foster, Christopher Saski, Guohai Wu, Dongfa Sun, and Hong Luo. "DRMY1, a Myb-Like Protein, Regulates Cell Expansion and Seed Production in Arabidopsis thaliana." Plant and Cell Physiology 60, no. 2 (October 23, 2018): 285–302. http://dx.doi.org/10.1093/pcp/pcy207.

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Abstract Plant organ development to a specific size and shape is controlled by cell proliferation and cell expansion. Here, we identify a novel Myb-like Arabidopsis gene, Development Related Myb-like1 (DRMY1), which controls cell expansion in both vegetative and reproductive organs. DRMY1 is strongly expressed in developing organs and its expression is reduced by ethylene while it is induced by ABA. DRMY1 has a Myb-like DNA-binding domain, which is predominantly localized in the nucleus and does not exhibit transcriptional activation activity. The loss-of-function T-DNA insertion mutant drmy1 shows reduced organ growth and cell expansion, which is associated with changes in the cell wall matrix polysaccharides. Interestingly, overexpression of DRMY1 in Arabidopsis does not lead to enhanced organ growth. Expression of genes involved in cell wall biosynthesis/remodeling, ribosome biogenesis and in ethylene and ABA signaling pathways is changed with the deficiency of DRMY1. Our results suggest that DRMY1 plays an essential role in organ development by regulating cell expansion either directly by affecting cell wall architecture and/or cytoplasmic growth or indirectly through the ethylene and/or ABA signaling pathways.

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Zhang, Lei, Deqin Feng, Wenxia Fang, Haomiao Ouyang, Yuanming Luo, Ting Du, and Cheng Jin. "Comparative proteomic analysis of an Aspergillus fumigatus mutant deficient in glucosidase I (AfCwh41)." Microbiology 155, no. 7 (July 1, 2009): 2157–67. http://dx.doi.org/10.1099/mic.0.027490-0.

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α-Glucosidase I regulates trimming of the terminal α-1,2-glucose residue in the N-glycan processing pathway, which plays an important role in quality control systems in mammalian cells. Previously, we identified the gene encoding α-glucosidase I in the opportunistic human fungal pathogen Aspergillus fumigatus, namely Afcwh41. Deletion of the Afcwh41 gene results in a severe reduction of conidia formation, a temperature-sensitive deficiency of cell wall integrity, and abnormalities of polar growth and septation. An upregulation of the genes encoding Rho-type GTPases was also observed, which suggests activation of the cell wall integrity pathway in the mutant. Using 2D gel analysis, we revealed that the proteins involved in protein assembly, ubiquitin-mediated degradation and actin organization are altered in the ΔAfcwh41 mutant. Evidence was obtained for a defect in the polarized localization of the actin cytoskeleton in the mutant. Our results suggest that blocking of the glucose trimming in A. fumigatus might induce accumulation of misfolded proteins in the endoplasmic reticulum; these misfolded proteins are probably required for cell wall synthesis and thus activate the cell wall integrity pathway, which then causes the abnormal polarity associated with the ΔAfcwh41 mutant.

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Zhang, Shu, Hanzhong Gao, Lixia Wang, Yihui Zhang, Dandan Zhou, Ali Anwar, Jingjuan Li, et al. "Comparative Transcriptome and Co-Expression Network Analyses Reveal the Molecular Mechanism of Calcium-Deficiency-Triggered Tipburn in Chinese Cabbage (Brassica rapa L. ssp. Pekinensis)." Plants 11, no. 24 (December 16, 2022): 3555. http://dx.doi.org/10.3390/plants11243555.

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Chinese cabbage tipburn is characterized by the formation of necrotic lesions on the margin of leaves, including on the insides of the leafy head. This physiological disorder is associated with a localized calcium deficiency during leaf development. However, little information is available regarding the molecular mechanisms governing Ca-deficiency-triggered tipburn. This study comprehensively analysed the transcriptomic comparison between control and calcium treatments (CK and 0 mM Ca) in Chinese cabbage to determine its molecular mechanism in tipburn. Our analysis identified that the most enriched gene ontology (GO) categories are photosynthesis, thylakoid and cofactor binding. Moreover, the KEGG pathway was most enriched in photosynthesis, carbon metabolism and carbon fixation. We also analyzed the co-expression network by functional categories and identified ten critical hub differentially expressed genes (DEGs) in each gene regulatory network (GRN). These DEGs might involve abiotic stresses, developmental processes, cell wall metabolism, calcium distribution, transcription factors, plant hormone biosynthesis and signal transduction pathways. Under calcium deficiency, CNX1, calmodulin-binding proteins and CMLs family proteins were downregulated compared to CK. In addition, plant hormones such as GA, JA, BR, Auxin and ABA biosynthesis pathways genes were downregulated under calcium treatment. Likewise, HATs, ARLs and TCP transcription factors were reported as inactive under calcium deficiency, and potentially involved in the developmental process. This work explores the specific DEGs’ significantly different expression levels in 0 mM Ca and the control involved in plant hormones, cell wall developments, a light response such as chlorophylls and photosynthesis, transport metabolism and defence mechanism and redox. Our results provide critical evidence of the potential roles of the calcium signal transduction pathway and candidate genes governing Ca-deficiency-triggered tipburn in Chinese cabbage.

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Lu, Zhifeng, Tao Ren, Jing Li, Wenshi Hu, Jianglin Zhang, Jinyao Yan, Xiaokun Li, Rihuan Cong, Shiwei Guo, and Jianwei Lu. "Nutrition-mediated cell and tissue-level anatomy triggers the covariation of leaf photosynthesis and leaf mass per area." Journal of Experimental Botany 71, no. 20 (July 29, 2020): 6524–37. http://dx.doi.org/10.1093/jxb/eraa356.

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Abstract Plants in nutrient-poor habitats converge towards lower rates of leaf net CO2 assimilation (Aarea); however, they display variability in leaf mass investment per area (LMA). How a plant optimizes its leaf internal carbon investment may have knock-on effects on structural traits and, in turn, affect leaf carbon fixation. Quantitative models were applied to evaluate the structural causes of variations in LMA and their relevance to Aarea in rapeseed (Brassica napus) based on their responses to nitrogen (N), phosphorus (P), potassium (K), and boron (B) deficiencies. Leaf carbon fixation decreased in response to nutrient deficiency, but the photosynthetic limitations varied greatly depending on the deficient nutrient. In comparison with Aarea, the LMA exhibited diverse responses, being increased under P or B deficiency, decreased under K deficiency, and unaffected under N deficiency. These variations were due to changes in cell- and tissue-level carbon investments between cell dry mass density (N or K deficiency) and cellular anatomy, including cell dimension and number (P deficiency), or both (B deficiency). However, there was a conserved pattern independent of nutrient-specific limitations—low nutrient availability reduced leaf carbon fixation but increased carbon investment in non-photosynthetic structures, resulting in larger but fewer mesophyll cells with a thicker cell wall but a lower chloroplast surface area appressed to the intercellular airspace, which reduced the mesophyll conductance and feedback-limited Aarea. Our results provide insight into the importance of mineral nutrients in balancing the leaf carbon economy by coordinating leaf carbon assimilation and internal distribution.

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Cho, J. H., Y. S. Oh, K. W. Park, J. Yu, K. Y. Choi, J. Y. Shin, D. H. Kim, et al. "Calsequestrin, a calcium sequestering protein localized at the sarcoplasmic reticulum, is not essential for body-wall muscle function in Caenorhabditis elegans." Journal of Cell Science 113, no. 22 (November 15, 2000): 3947–58. http://dx.doi.org/10.1242/jcs.113.22.3947.

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Calsequestrin is the major calcium-binding protein of cardiac and skeletal muscles whose function is to sequester Ca(2+)in the lumen of the sarcoplasmic reticulum (SR). Here we describe the identification and functional characterization of a C. elegans calsequestrin gene (csq-1). CSQ-1 shows moderate similarity (50% similarity, 30% identity) to rabbit skeletal calsequestrin. Unlike mammals, which have two different genes encoding cardiac and fast-twitch skeletal muscle isoforms, csq-1 is the only calsequestrin gene in the C. elegans genome. We show that csq-1 is highly expressed in the body-wall muscles, beginning in mid-embryogenesis and maintained through the adult stage. In body-wall muscle cells, CSQ-1 is localized to sarcoplasmic membranes surrounding sarcomeric structures, in the regions where ryanodine receptors (UNC-68) are located. Mutation in UNC-68 affects CSQ-1 localization, suggesting that the two possibly interact in vivo. Genetic analyses of chromosomal deficiency mutants deleting csq-1 show that CSQ-1 is not essential for initiation of embryonic muscle formation and contraction. Furthermore, double-stranded RNA injection resulted in animals completely lacking CSQ-1 in body-wall muscles with no observable defects in locomotion. These findings suggest that although CSQ-1 is one of the major calcium-binding proteins in the body-wall muscles of C. elegans, it is not essential for body-wall muscle formation and contraction.

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Pan, Yuan, Zhenhua Wang, Lu Yang, Zhifang Wang, Lei Shi, Radnaa Naran, Parastoo Azadi, and Fangsen Xu. "Differences in cell wall components and allocation of boron to cell walls confer variations in sensitivities of Brassica napus cultivars to boron deficiency." Plant and Soil 354, no. 1-2 (November 29, 2011): 383–94. http://dx.doi.org/10.1007/s11104-011-1074-6.

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Hamdin, Candra D., Meng-Ling Wu, Chen-Mei Chen, Yen-Chun Ho, Wei-Cheng Jiang, Pei-Yu Gung, Hua-Hui Ho, Huai-Chia Chuang, Tse-Hua Tan, and Shaw-Fang Yet. "Dual-Specificity Phosphatase 6 Deficiency Attenuates Arterial-Injury-Induced Intimal Hyperplasia in Mice." International Journal of Molecular Sciences 24, no. 24 (December 5, 2023): 17136. http://dx.doi.org/10.3390/ijms242417136.

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In response to injury, vascular smooth muscle cells (VSMCs) of the arterial wall dedifferentiate into a proliferative and migratory phenotype, leading to intimal hyperplasia. The ERK1/2 pathway participates in cellular proliferation and migration, while dual-specificity phosphatase 6 (DUSP6, also named MKP3) can dephosphorylate activated ERK1/2. We showed that DUSP6 was expressed in low baseline levels in normal arteries; however, arterial injury significantly increased DUSP6 levels in the vessel wall. Compared with wild-type mice, Dusp6-deficient mice had smaller neointima. In vitro, IL-1β induced DUSP6 expression and increased VSMC proliferation and migration. Lack of DUSP6 reduced IL-1β-induced VSMC proliferation and migration. DUSP6 deficiency did not affect IL-1β-stimulated ERK1/2 activation. Instead, ERK1/2 inhibitor U0126 prevented DUSP6 induction by IL-1β, indicating that ERK1/2 functions upstream of DUSP6 to regulate DUSP6 expression in VSMCs rather than downstream as a DUSP6 substrate. IL-1β decreased the levels of cell cycle inhibitor p27 and cell–cell adhesion molecule N-cadherin in VSMCs, whereas lack of DUSP6 maintained their high levels, revealing novel functions of DUSP6 in regulating these two molecules. Taken together, our results indicate that lack of DUSP6 attenuated neointima formation following arterial injury by reducing VSMC proliferation and migration, which were likely mediated via maintaining p27 and N-cadherin levels.

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Journal articles on the topic 'Cell wall deficiency'

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