Changes In Wall Structure Research Articles

Occurrence of early softening in papaya due to specific cell wall-related changes

This study aims to find characteristics that might explain the rapid softening disorder in papaya. At the time of harvest, it was observed that papaya with early softening disorder (ESD) and those without the disorder could not be distinguished exclusively on the basis of their skin color and pulp firmness. Fruit with ESD and without ESD were harvested at maturity stage 1 and evaluated for 10 d at 10 °C, according to the softening index (SI) methodology. The symptoms of early softening disorder were clearly observed between 2 d and 8 d of storage, with firmness 71% lower than the initial firmness, presenting atypical behavior for fruit stored under refrigeration. There was no difference between the fruit with and without ESD for soluble solids contents, but titratable acidity and ascorbic acid were significantly different between both stages of fruit that could be associated with the ripening patterns. Furthermore, there were no differences between fruit with ESD and those without ESD in respiratory rate and ethylene production under refrigerated storage, what suggested that the occurrence of disorder was not related to an increase in ethylene post-harvest period. This work provided evidence to discriminate fruit susceptible to suffer from ESD from those not susceptible to this disorder. The cell wall polysaccharide fractions indicated significant differences between fruit with ESD and without ESD at the moment of harvest suggesting modifications in the cellulose-hemicellulose domain. Moreover, the ethylene production did not follow cell wall modification, suggesting that changes in the cell wall structure could have happened during fruit growth. In this way, depending on the intensity of the cell wall modification, the fruit will exhibit the flesh early softening after harvest.

Morphologic and Morphometric Evaluation of the Carotid Artery Wall: A Cadaver-Based Light and Scanning Electron Microscopic Study

Introduction: A variety of changes occur on the elastic artery wall with age. Ultrastructural studies made in this area are mostly animal based. We aimed to evaluate wall changes and three-dimensional organization of the elastic lamellae with aging in humans. Material and Methods: Common carotid arteries were obtained from 17 human cadavers which were grouped as G1 (n = 6), 30–39 years; G2 (n = 5), 40–49 years; and G3 (n = 6), >50 years of age. Samples were evaluated under light and scanning electron microscopes. Results: Examination of G1 revealed intimal thickening and foamy cell infiltration. G2 and G3 had plaques bulging into the lumen and interlamellar space was widened. The lamellae were more straight. There was a positive correlation between intimal thickness and age. Elastic fiber content decreased with aging. Scanning electron microscopic analysis confirmed the findings. G1 and G2 had a smooth surfaced internal elastic lamina with uniform fenestrations whereas G3 contained numerous irregular fenestrae. Discussion and Conclusion: With this study, we showed some other wall structure changes beside plaque formation by aging. Which layer is affected the most was not clear at previous clinical studies because using ultrasonography (USG) cannot address the layer. Microscopic evaluation of this study revealed that when a wall thickening is detected by USG, it is due to intimal thickening. The specific vessel layer structural changes are important for proper treatment.

THESEUS1 modulates cell wall stiffness and abscisic acid production in Arabidopsis thaliana

Plant cells can be distinguished from animal cells by their cell walls and high-turgor pressure. Although changes in turgor and the stiffness of cell walls seem coordinated, we know little about the mechanism responsible for coordination. Evidence has accumulated that plants, like yeast, have a dedicated cell wall integrity maintenance mechanism. It monitors the functional integrity of the wall and maintains integrity through adaptive responses induced by cell wall damage arising during growth, development, and interactions with the environment. These adaptive responses include osmosensitive induction of phytohormone production, defense responses, as well as changes in cell wall composition and structure. Here, we investigate how the cell wall integrity maintenance mechanism coordinates changes in cell wall stiffness and turgor in Arabidopsis thaliana We show that the production of abscisic acid (ABA), the phytohormone-modulating turgor pressure, and responses to drought depend on the presence of a functional cell wall. We find that the cell wall integrity sensor THESEUS1 modulates mechanical properties of walls, turgor loss point, ABA biosynthesis, and ABA-controlled processes. We identify RECEPTOR-LIKE PROTEIN 12 as a component of cell wall integrity maintenance-controlling, cell wall damage-induced jasmonic acid (JA) production. We propose that THE1 is responsible for coordinating changes in turgor pressure and cell wall stiffness.

Purification, characterization, and antifungal activity of Bacillus cereus strain NK91 chitinase from rhizospheric soil samples of Himachal Pradesh, India.

Newly isolated Bacillus cereus strain NK91 was characterized for extracellular chitinase production. Partially purified chitinase showed a molecular weight of 43.7 kDa in SDS-PAGE analysis. The optimum pH and temperature for the partially purified enzyme were 7.0 and 40°C, respectively. The addition of Mn2+ resulted in a 21% increase in enzyme activity as compared to the control. The Vmax and Km of the enzyme were determined as 76.9 μmol/min and 0.07 mg/mL, respectively. This enzyme exhibited stronger antifungal activity towards Fusarium oxysporum (66.7%), Rhizoctonia solani (64.6%), and Colletotrichum gloeosporioides (63%), and transmission electron microscopy and scanning transmission electron microscopy analysis showed considerable changes in cell wall structure with the treatment of purified chitinase as compared to control. Therefore, this enzyme reveals its biocontrol potential against potent phytopathogens in agriculture that can be helpful in swapping harmful as well as expensive fungicides.

Vasoprotective effects hypotensive therapy in patients with coronary heart disease combined with chronic kidney disease stage 2-3 after coronary stenting

Aim To study the condition of coronary vasculature by data of coronarography (CG) in patients with chronic ischemic heart disease (IHD) and arterial hypertension (AH) associated with stage 2-4 chronic kidney disease (CKD) and to evaluate the effect of a 12-week complex treatment with perindopril or with a combination of perindopril/amlodipine on changes in vascular wall stiffness, endothelial function, and structure and function parameters in this patient category after coronary stenting.Material and methodsr This study included 87 patients with chronic IHD and AH associated with stage 2-3 CKD for whom CG was performed due to ineffectiveness of the antianginal therapy. The patients were divided into three subgroups: subgroup 1 included 28 patients who received a conservative treatment with perindopril 10 mg/day; subgroup 2 consisted of 25 patients who underwent coronary stenting and were prescribed perindopril; subgroup 3 consisted of 34 patients who underwent stenting and were prescribed the perindopril/amlodipine combination. The reference group included 47 patients with IHD and AH with preserved kidney function. Anatomic and functional parameters of the heart, arterial stiffness, pulse wave velocity, cardio-ankle vascular index, augmentation index, central aortic systolic and pulse pressure, endothelium-dependent vasodilation, plasma concentration of endothelin-1 (ET-1), and plasma concentration of nitric oxide metabolites were evaluated at baseline and after 12 weeks of treatment.Results In patients with IHD, AH, and stage 2-3 CKD, arterial stiffness was more pronounced than in patients with preserved kidney function. Concentrations of ET-1 were significantly higher and levels of nitric oxide were lower in CKD. Supplementing the complex therapy with perindopril resulted in a considerable hypotensive effect in all subgroups, improvement of the kidney function, and positive dynamics of arterial stiffness and endothelial function. Changes in these parameters were more pronounced in patients after coronary stenting than in patients receiving only a conservative treatment. The use of perindopril/amlodipine following stenting exerted the most significant angioprotective and cardioprotective effect.Conclusion Patients with IHD and AH in combination with early CKD have pronounced impairment of the condition of arterial blood vessels and the heart. Addition of perindopril to the treatment not only exerted a hypotensive effect but also beneficially influenced mechanisms of progression of this combined pathology.

Human herpesvirus DNA occurrence in intracranial aneurysmal wall: illustrative case

BACKGROUNDSubarachnoid hemorrhages secondary to intracranial aneurysms (IAs) are events of high mortality. These neurological vascular diseases arise from local and systemic inflammation that culminates in vessel wall changes. They may also have a possible relationship with chronic viral infections, such as human herpesvirus (HHV), and especially Epstein–Barr virus (EBV), which causes several medical conditions. This is the first description of the presence of HHV deoxyribonucleic acid (DNA) in a patient with IA.OBSERVATIONSA 61-year-old woman with a downgraded level of consciousness underwent radiological examinations that identified a 10-mm ruptured aneurysm in the anterior communicating artery. A microsurgery clip was performed to definitively treat the aneurysm and occurred without surgical complications. Molecular analysis of the material obtained revealed the presence of EBV DNA in the aneurysm wall. The patient died 21 days after admission due to clinical complications and brain swelling.LESSONSThis is the first description of the presence of herpesvirus DNA in a patient with IA, presented in 2.8% of our data. These findings highlight that viral infection may contribute to the pathophysiology and is an additional risk factor for IA formation, progression, and rupture by modulating vessel wall inflammation and structural changes in chronic infections.

P2X7 Receptor Blockade Protects Against Acrolein-Induced Bladder Damage: A Potential New Therapeutic Approach for the Treatment of Bladder Inflammatory Diseases.

Inflammatory conditions of the urinary bladder have been shown to be associated with urothelial damage and loss of function. The purinergic P2X7 receptor has been implicated in several inflammatory conditions. The aim of this study was to investigate the role of the P2X7 receptor in acrolein-induced inflammatory damage using the porcine urinary bladder. For this purpose, an ex-vivo model of porcine urothelial damage induced by direct instillation of acrolein into the whole bladder lumen was used. To determine the role of the P2X7 receptor, the bladders were pre-incubated with a selective P2X7 receptor antagonist, A804598 (10 μM), for 1 h. The effects of the acrolein-induced urothelial damage on the bladder’s function were assessed by examining the bladder wall contractile response, structure changes, apoptosis, and oxidative stress in the bladder tissues. The acrolein treatment led to significant damage to the urothelium histology, tight junction expression, and contractile responses. Acrolein also induced apoptosis in the mucosa layer. All these acrolein-induced responses were attenuated by pre-treatment with the P2X7 receptor antagonist A804598. Acrolein also significantly induced DNA oxidation in the submucosal layer; however, the P2X7 receptor antagonism did not show any protective effect towards the acrolein-induced oxidative stress. These findings suggested that the P2X7 receptor is involved in the acrolein-induced damage to the urothelium; therefore, the P2X7 receptor antagonists may be a new therapeutic option for the treatment of bladder inflammation.

Aorta wall, myocardial and brain structural parallel changes in early stage of experimental atherosclerosis

Aorta wall, myocardial and brain structural parallel changes in early stage of experimental atherosclerosis

Characterization of contrasting rice (Oryza sativa L.) genotypes reveals the Pi-efficient schema for phosphate starvation tolerance

BackgroundPhosphorus (P), being one of the essential components of nucleic acids, cell membranes and enzymes, indispensable for diverse cellular processes like photosynthesis/carbohydrate metabolism, energy production, redox homeostasis and signaling. Crop yield is severely affected due to Phosphate (Pi) deficiency; and to cope with Pi-deficiency, plants have evolved several strategies. Some rice genotypes are compatible with low Pi availability, whereas others are sensitive to Pi deficiency. However, the underlying molecular mechanism for low Pi tolerance remains largely unexplored.ResultSeveral studies were carried out to understand Pi-deficiency responses in rice at seedling stage, but few of them targeted molecular aspects/responses of Pi-starvation at the advanced stage of growth. To delineate the molecular mechanisms for low Pi tolerance, a pair of contrasting rice (Oryza sativa L.) genotypes [viz. Pusa-44 (Pi-deficiency sensitive) and its near isogenic line (NIL-23, Pi-deficiency tolerant) harboring Phosphorus uptake 1 (Pup1) QTL from an aus landrace Kasalath] were used. Comparative morphological, physiological, and biochemical analyses confirmed some of the well-known findings. Transcriptome analysis of shoot and root tissues from 45-day-old rice plants grown hydroponically under P-sufficient (16 ppm Pi) or P-starved (0 ppm Pi) medium revealed that Pi-starvation stress causes global transcriptional reprogramming affecting several transcription factors, signaling pathways and other regulatory genes. We could identify several significantly up-regulated genes in roots of NIL-23 under Pi-starvation which might be responsible for the Pi starvation tolerance. Pathway enrichment analysis indicated significant role of certain phosphatases, transporters, transcription factors, carbohydrate metabolism, hormone-signaling, and epigenetic processes in improving P-starvation stress tolerance in NIL-23.ConclusionWe report the important candidate mechanisms for Pi acquisition/solubilization, recycling, remobilization/transport, sensing/signalling, genetic/epigenetic regulation, and cell wall structural changes to be responsible for P-starvation tolerance in NIL-23. The study provides some of the novel information useful for improving phosphorus-use efficiency in rice cultivars.

Intimal thickening and disruption of the media occur in the arterial walls of coronary arteries not associated with coronary arterial aneurysms in patients with Kawasaki disease

BackgroundCoronary artery aneurysm (CAA) is an important complication of Kawasaki disease (KD) that is associated with arterial structure damage. However, few studies have examined structural changes in coronary arteries that are not associated with CAA.MethodsWe examined coronary arteries in KD patients with CAAs who underwent follow-up coronary angiography (CAG) and optical coherence tomography (OCT). Coronary arterial branches with no abnormal findings during the most recent CAG were classified into two groups. Arteries with an acute-phase CAA that later regressed were classified as group R; arteries with no abnormal findings on either acute or convalescent phase CAG were classified as group N. Coronary arterial wall structural changes were compared between groups using OCT.ResultsFifty-seven coronary arterial branches in 23 patients were evaluated by OCT. Thirty-six branches showed no abnormality during the most recent CAG. Both groups R and N comprised 18 branches. Maximum intimal thicknesses in groups R and N were 475 and 355 µm, respectively (p = 0.007). The incidences of media disruption were 100% and 67%, respectively (p = 0.02). Calcification, macrophage accumulation, and thrombus were not found in either group.ConclusionsIntimal thickening and disruption of the media occur in coronary arteries with acute phase CAAs that later regress in the convalescent phase, as well as in arteries with normal CAG findings in the acute and convalescent phases.

The zinc cluster transcription factor Czf1 regulates cell wall architecture and integrity in Candida albicans.

The fungal cell wall is essential for the maintenance of cellular integrity and mediates interactions of the cells with the environment. It is a highly flexible organelle whose composition and organization is modulated in response to changing growth conditions. In the pathogenic yeast Candida albicans, a network of signaling pathways regulates the structure of the cell wall, and mutants with defects in these pathways are hypersensitive to cell wall stress. By harnessing a library of genetically activated forms of all C.albicans zinc cluster transcription factors, we found that a hyperactive Czf1 rescued the hypersensitivity to cell wall stress of different protein kinase deletion mutants. The hyperactive Czf1 induced the expression of many genes with cell wall-related functions and caused visible changes in the cell wall structure. C.albicans czf1Δ mutants were hypersensitive to the antifungal drug caspofungin, which inhibits cell wall biosynthesis. The changes in cell wall architecture caused by hyperactivity or absence of Czf1 resulted in an increased recognition of C.albicans by human neutrophils. Our results show that Czf1, which is known as a regulator of filamentous growth and white-opaque switching, controls the expression of cell wall genes and modulates the architecture of the cell wall.

Ecotoxicological effects of new generation pollutants (nanoparticles, amoxicillin and white musk) on freshwater and marine phytoplankton species

Phytoplankton occupies a key trophic level in aquatic ecosystems. Chemical impacts on these primary producers can disrupt the integrity of an entire ecosystem. Two freshwater (Pseudokirchneriella subcapitata-Ps and Scenedesmus obliquus-S) and three marine (Phaeodactylum tricornutum-P, Isochrysis galbana-I, Tetraselmis suecica-T) microalgae species were exposed to dilutions of four chemicals: nanoparticles (n-TiO2, n-ZnO), amoxicillin (antibiotic), and white musk (personal care fragrance) to determine the half maximal effective concentration (EC50) after 72 h of exposure under standardized and controlled environmental conditions. Cell cultures were exposed to EC50 to determine sublethal effects (72 h) based on biochemical (chlorophylls a, b, c), molecular (changes in outer cell wall structure), and morphological alterations. We report for the first time EC50 values for nanoparticles in not standardized species (S, I and T) and for amoxicillin and white musk in all tested species. Standardized species (Ps and P) were less sensitive than non-standardized in some cases. Fourier-transformed infrared spectroscopy showed a marked spectral alteration (from 10.44% to 90.93%) of treated cultures compared to negative controls; however, principal component analysis disclosed no differences in molecular alteration between the five microalgae species or the two aquatic habitats considered. There was a significant decrease in chlorophylls content in all species exposed to EC50 compared to controls (Kruskal Wallis test; p < 0.05). There was a significant increase in cell-size (Mann–Whitney U test; p < 0.05) in I, P and T exposed to white musk and S exposed to amoxicillin. Findings highlight ecotoxicological risks from new generation pollutants for primary producers in aquatic ecosystems.

Study on the pathophysiological mechanism responsible for lower urinary tract symptoms associated with prostate cancer using an animal model.

To investigate the pathophysiological mechanism leading to lower urinary tract symptoms in prostate cancer (PCa) by using an animal model. An orthotopic PCa model in mice was established by injection of human DU145 cells into the prostate gland lateral lobe of NOD.CB17-Prkdcscid /NcrCrlBltw (NOD-SCID) mice. Cancer growth was quantified by a luciferase-based in vivo imaging system (IVIS) serially every 7 days. Comparisons were made for urodynamic parameters, bladder histology, and biological markers until the sixth week. Bladder wall structural changes were assessed by the bladder wall thickness and degree of fibrosis. Biomarker expressions in bladder tissue including muscarinic acetylcholine receptor 2 (M2 ), transient receptor potential cation channel subfamily V member 4 (TRPV4), BCL2-associated X protein (Bax), and caspase3 were evaluated by immunohistochemical staining and immunofluorescence confocal laser scanning microscopy. DU145 cell growth in the prostate was successfully monitored by a luciferase-based IVIS. after orthotopic injection. Using our injection technique, no anatomical obstruction of the bladder outlet and urethra was noted up to 6 weeks after injection. The presence of PCa induced changes in urinary bladder histology, biomarkers, and urodynamic parameters. Cystometry showed features of detrusor overactivity with increased voiding frequency and high-amplitude voiding contractions from the fourth week onward. Histological analyses 4 weeks after DU145 injection demonstrated detrusor thickening and bladder wall fibrosis. Immunohistochemistry showed increased expressions of bladder M2 , TRPV4, Bax, and caspase3 in the PCa mice as early as in the first or second week. PCa can induce bladder microenvironment changes involving neural receptors and biological mediators leading to histological and functional alterations even in the absence of overt anatomical obstruction.

Silver nanoparticles (AgNPs) internalization and passage through the Lactuca sativa (Asteraceae) outer cell wall.

Silver nanoparticle (AgNPs) toxicity is related to nanoparticle interaction with the cell wall of microorganisms and plants. This interaction alters cell wall conformation with increased reactive oxygen species (ROS) in the cell. With the increase of ROS in the cell, the dissolution of zero silver (Ag0) to ionic silver (Ag+) occurs, which is a strong oxidant agent to the cellular wall. AgNP interaction was evaluated by transmission electron microscopy (TEM) on Lactuca sativa roots, and the mechanism of passage through the outer cell wall (OCW) was also proposed. The results suggest that Ag+ binds to the hydroxyls (OH) present in the cellulose structure, thus causing the breakdown of the hydrogen bonds. Changes in cell wall structure facilitate the passage of AgNPs, reaching the plasma membrane. According to the literature, silver nanoparticles with an average diameter of 15nm are transported across the membrane into the cells by caveolines. This work describes the interaction between AgNPs and the cell wall and proposes a transport model through the outer cell wall.

The relationship between fluoride accumulation in tea plant and changes in leaf cell wall structure and composition under different fluoride conditions

Tea plant is capable of hyper-accumulating fluoride (F) in leaves, suggesting drinking tea may cause excessive F intake in our body and threaten the health. This study investigated the changes in the structure, composition, and F content in the leaf cell wall of the tea (Camellia sinensis) under different F conditions to demonstrate the role of cell wall in F enrichment in tea plants. The cell wall was shown as the main part for F accumulation (67%-92%), with most of F distributed in the pectin fraction (56%-71%). With increasing F concentration, a significant increase (p<0.05) was observed in the F content of cell wall and its components, the level of cell wall metal ions (i.e. Cu, Mg, Zn, Al, Ca, Ba, Mn), as well as the content of total cell wall materials, cellulose, and pectin. Meanwhile, the level of Cu, Mg, Zn, pectin, and cellulose was significantly positively correlated with the F content in the leaf cell wall. F addition was shown to increase the fluorescence intensity of LM19 and 2F4 antibody-labeled low-methylesterified homogalacturonans (HGs), while decrease LM20-labeled high-methylesterified HGs, coupled with an increase in the activity and gene expression of pectin methyl esterases (PMEs) in tea leaves. All these results suggest that F addition can increase pectin content and demethylesterification, leading to increased absorption of metal cations and chelation of F in the cell wall through the action of metal ions.

Changes in cell wall structure and protein set in Candida maltosa grown on hexadecane.

The yeast Candida maltosa is a model organism for studying adaptive changes in the structure and function of the cell wall when consuming water-insoluble nutrient sources. The cells of C. maltosa that utilize hydrocarbons contain supramolecular structures, so-called "canals" in the cell wall. Differences in protein profiles of culture liquids and cell wall extracts of C. maltosa grown on glucose and hexadecane were analyzed. Three proteins specific of cells grown on hexadecane were revealed using mass spectrometry: glycosyl hydrolase EPD2 in the culture liquid; a protein belonging to the cytochrome C family in the 0.5 mol/L NaCl extract; and PPIA_CANAL protein known as chaperone, in the 0.1% SDS extract. The possible role of these proteins in cell wall structures responsible for adaptation to hexadecane utilization is discussed.

Remodeling of the Heart of the Premature Child

Epidemiological studies consistently have suggested an association between low birth weight and increased rate of cardiovascular morbidity and mortality in adult life. Preterm birth, as one of the leading causes of the low birth weight, is associated with cardiovascular remodeling which consists of changes in heart chambers geometry and contraction-relaxation mode, ventricular hypertrophy, arterial wall structure and density changes. Several types of preterm birth are discussed: prematurity, associated with placental insufficiency and fetal growth restriction, preterm leaking of amniotic fluid, and twin pregnancy. DNA methylation process under the influence of epigenetic factors of the intrauterine and early postnatal development is suggested as a one of the main mechanism of cardiovascular remodeling in preterm infants. The other mechanisms of cardiovascular remodeling are discussed in terms of the modern intrauterine programming concept. The early diagnostics and prevention of cardiovascular diseases in preterm born children are discussed. The treatment during prenatal and early postnatal periods as well as prevention of the remodeling causes could diminish and even reverse the development of the negative cardiovascular events and diseases in later life according to the so called concept of one thousand days opportunities window.

Cyanidin-3-O-glucoside attenuates endothelial cell dysfunction by modulating miR-204-5p/SIRT1-mediated inflammation and apoptosis.

Endothelial cell (EC) dysfunction is a major symptom associated with the initiation of atherosclerosis (AS). Cyanidin-3-O-glucoside (C3G) has the potentials to attenuate AS symptoms. In the current study, the mechanism driving the effects of C3G on AS rabbits and injured ECs were explored by focusing on the changes in miR-204-5p/SIRT1 axis. AS symptoms were induced in rabbits using high-fatty diet (HFD) plus balloon catheter injured method and handled with C3G of two doses. Then the changes in artery wall structure, hemodynamics parameters, blood lipid level, systemic inflammation, and miR-204-5p/SIRT1 axis were detected. EC dysfunction was imitated by subjecting human umbilical vein endothelial cells (HUVECs) to TNF-α, which was then handled with C3G. The changes in apoptosis, inflammation, and miR-204-5p/SIRT1 axis were detected. The results showed that the administrations of C3G improved artery wall structure and hemodynamics parameters, decreased blood lipid levels, and suppressed pro-inflammatory cytokine production in HFD rabbits, which was associated with the down-regulation of miR-204-5p and the up-regulation of SIRT1. In in vitro assays, the treatments of C3G suppressed apoptosis, inhibited inflammation, down-regulated miR-204-5p level, and induced SIRT1 level in HUVECs. The overexpression of miR-204-5p impaired the protective effects of C3G on the injured HUVECs by increasing cell apoptosis and inflammation. The findings outlined in the current study confirmed the protective effects of C3G on EC function, which was associated with the down-regulation of miR-204-5p and the up-regulation of SIRT1.

Do Cell Wall Esters Facilitate Forest Response to Climate?

Terrestrial ecosystem dynamics are strongly modified by stresses associated with climate change, impacting plant growth and development, mortality, and ecological succession. Here we highlight the potential role of plant cell wall esters to link changes in cell wall structure and function with biosphere-atmosphere fluxes of methanol, acetic acid, carbon dioxide (CO2), and water (H2O).

Cell wall structural changes lead to separation and shedding of biofouled epidermal cell wall layers by the brown alga Ascophyllum nodosum.

Marine plants control the accumulation of biofouling organisms (epibionts) on their surfaces by various chemical and physical means. Ascophyllum nodosum is a perennial multicellular brown alga known to shed patches of epidermal material, thus removing epibionts and exposing unfouled surfaces to another cycle of colonization. While surface shedding is documented in multiple marine macroalgae, the cell and developmental biology of the phenomenon is almost unexplored. A previous investigation of Ascophyllum not only revealed regular cycles of epibiont accumulation and epidermal shedding but also stimulated the development of methods to detect the corresponding changes in epidermal (meristoderm) cells that are reported here. Confocal laser scanning microscopy of cell walls and cytoplasm fluorescently stained with Solophenyl Flavine 7GFE (Direct Yellow 96) and the lipophilic dye Rhodamine B (respectively) was combined with light and electron microscopy of chemically fixed or freeze-substituted tissues. As epibionts accumulated, epidermal cells generated thick, apical cell walls in which differentially stained central layers subsequently developed, marking the site of future cell wall separation. During cell wall separation, the outermost part of the cell wall and its epibionts plus the upper parts of the anticlinal walls between neighboring cells detached in a layer from multiple epidermal cells, exposing the remaining inner part of the cell wall to new colonizing organisms. These findings highlight the dynamic nature of apical cell wall structure and composition in response to colonizing organisms and lay a foundation for further investigations on the periodic removal of biofouling epibionts from the surface of Ascophyllum fronds.