scholarly journals Towards elucidation of dynamic structural changes of plant thylakoid architecture

2012 ◽  
Vol 367 (1608) ◽  
pp. 3515-3524 ◽  
Author(s):  
Jan M. Anderson ◽  
Peter Horton ◽  
Eun-Ha Kim ◽  
Wah Soon Chow

Long-term acclimation of shade versus sun plants modulates the composition, function and structural organization of the architecture of the thylakoid membrane network. Significantly, these changes in the macroscopic structural organization of shade and sun plant chloroplasts during long-term acclimation are also mimicked following rapid transitions in irradiance: reversible ultrastructural changes in the entire thylakoid membrane network increase the number of grana per chloroplast, but decrease the number of stacked thylakoids per granum in seconds to minutes in leaves. It is proposed that these dynamic changes depend on reversible macro-reorganization of some light-harvesting complex IIb and photosystem II supracomplexes within the plant thylakoid network owing to differential phosphorylation cycles and other biochemical changes known to ensure flexibility in photosynthetic function in vivo. Some lingering grana enigmas remain: elucidation of the mechanisms involved in the dynamic architecture of the thylakoid membrane network under fluctuating irradiance and its implications for function merit extensive further studies.

Author(s):  
S. Phyllis Steamer ◽  
Rosemarie L. Devine

The importance of radiation damage to the skin and its vasculature was recognized by the early radiologists. In more recent studies, vascular effects were shown to involve the endothelium as well as the surrounding connective tissue. Microvascular changes in the mouse pinna were studied in vivo and recorded photographically over a period of 12-18 months. Radiation treatment at 110 days of age was total body exposure to either 240 rad fission neutrons or 855 rad 60Co gamma rays. After in vivo observations in control and irradiated mice, animals were sacrificed for examination of changes in vascular fine structure. Vessels were selected from regions of specific interest that had been identified on photomicrographs. Prominent ultrastructural changes can be attributed to aging as well as to radiation treatment. Of principal concern were determinations of ultrastructural changes associated with venous dilatations, segmental arterial stenosis and tortuosities of both veins and arteries, effects that had been identified on the basis of light microscopic observations. Tortuosities and irregularly dilated vein segments were related to both aging and radiation changes but arterial stenosis was observed only in irradiated animals.


2017 ◽  
Vol 43 (4) ◽  
pp. 511-516
Author(s):  
Joel Hanhart ◽  
Yishay Weill ◽  
Yaakov Rozenman

Bone ◽  
1992 ◽  
Vol 13 (6) ◽  
pp. 417-422 ◽  
Author(s):  
C.H. Turner ◽  
T.A. Woltman ◽  
D.A. Belongia

Blood ◽  
1965 ◽  
Vol 25 (6) ◽  
pp. 885-896 ◽  
Author(s):  
RICHARD A. RIFKIND ◽  
DAVID DANON

Abstract The ultrastructural changes in red blood cells exposed to phenylhydrazine, either in vivo or in vitro, are described. There is an age-dependent gradient of red cell sensitivity to this drug which includes the more mature reticulocytes as well as the population of circulating erythrocytes. Oxidative denaturation of hemoglobin and the formation of Heinz bodies, which constitute the major drug-induced lesion, are accompanied by a regular sequence of structural changes commencing in the central cytoplasm of erythrocytes and the drug-sensitive reticulocytes. These early changes often appear in close associaion with clusters of mitochondria. The initial morphologic lesion has an apparently crystalline structure and the significance of this stage is discussed. Heinz bodies grow by coalescence and condensation and finally come to lie just beneath the cell surface. Here they result in considerable distortion of cell shape and deformation of the plasma membrane. Thus, phenylhydrazine administration produces in red blood cells extensive ultrastructural alterations both in hemoglobin and in the cell membrane which may have considerable bearing on the fate of these cells in the circulation.


2020 ◽  
Vol 147 (1) ◽  
pp. 107-124
Author(s):  
Keiji Nishioka ◽  
Yusuke Kato ◽  
Shin-ichiro Ozawa ◽  
Yuichiro Takahashi ◽  
Wataru Sakamoto

AbstractProtein phosphorylation is a fundamental post-translational modification in all organisms. In photoautotrophic organisms, protein phosphorylation is essential for the fine-tuning of photosynthesis. The reversible phosphorylation of the photosystem II (PSII) core and the light-harvesting complex of PSII (LHCII) contribute to the regulation of photosynthetic activities. Besides the phosphorylation of these major proteins, recent phosphoproteomic analyses have revealed that several proteins are phosphorylated in the thylakoid membrane. In this study, we utilized the Phos-tag technology for a comprehensive assessment of protein phosphorylation in the thylakoid membrane of Arabidopsis. Phos-tag SDS-PAGE enables the mobility shift of phosphorylated proteins compared with their non-phosphorylated isoform, thus differentiating phosphorylated proteins from their non-phosphorylated isoforms. We extrapolated this technique to two-dimensional (2D) SDS-PAGE for detecting protein phosphorylation in the thylakoid membrane. Thylakoid proteins were separated in the first dimension by conventional SDS-PAGE and in the second dimension by Phos-tag SDS-PAGE. In addition to the isolation of major phosphorylated photosynthesis-related proteins, 2D Phos-tag SDS-PAGE enabled the detection of several minor phosphorylated proteins in the thylakoid membrane. The analysis of the thylakoid kinase mutants demonstrated that light-dependent protein phosphorylation was mainly restricted to the phosphorylation of the PSII core and LHCII proteins. Furthermore, we assessed the phosphorylation states of the structural domains of the thylakoid membrane, grana core, grana margin, and stroma lamella. Overall, these results demonstrated that Phos-tag SDS-PAGE is a useful biochemical tool for studying in vivo protein phosphorylation in the thylakoid membrane protein.


2020 ◽  
Vol 2 (1) ◽  
Author(s):  
Ian Grierson ◽  
Don Minckler ◽  
Marian K. Rippy ◽  
Andrew J. Marshall ◽  
Nathalie Collignon ◽  
...  

Abstract Background A major challenge for any glaucoma implant is their ability to provide long-term intraocular pressure lowering efficacy. The formation of a low-permeability fibrous capsule around the device often leads to obstructed drainage channels, which may impair the drainage function of devices. These foreign body-related limitations point to the need to develop biologically inert biomaterials to improve performance in reaching long-term intraocular pressure reduction. The aim of this study was to evaluate in vivo (in rabbits) the ocular biocompatibility and tissue integration of a novel suprachoroidal microinvasive glaucoma implant, MINIject™ (iSTAR Medical, Wavre, Belgium). Results In two rabbit studies, no biocompatibility issue was induced by the suprachoroidal, ab-externo implantation of the MINIject™ device. Clinical evaluation throughout the 6 post-operative months between the sham and test groups were similar, suggesting most reactions were related to the ab-externo surgical technique used for rabbits, rather than the implant material itself. Histological analysis of ocular tissues at post-operative months 1, 3 and 6 revealed that the implant was well-tolerated and induced only minimal fibroplasia and thus minimal encapsulation around the implant. The microporous structure of the device became rapidly colonized by cells, mostly by macrophages through cell migration, which do not, by their nature, impede the flow of aqueous humor through the device. Time-course analysis showed that once established, pore colonization was stable over time. No fibrosis nor dense connective tissue development were observed within any implant at any time point. The presence of pore colonization may be the process by which encapsulation around the implant is minimized, thus preserving the permeability of the surrounding tissues. No degradation nor structural changes of the implant occurred during the course of both studies. Conclusions The novel MINIject™ microinvasive glaucoma implant was well-tolerated in ocular tissues of rabbits, with observance of biointegration, and no biocompatibility issues. Minimal fibrous encapsulation and stable cellular pore colonization provided evidence of preserved drainage properties over time, suggesting that the implant may produce a long-term ability to enhance aqueous outflow.


PLoS ONE ◽  
2021 ◽  
Vol 16 (6) ◽  
pp. e0252649
Author(s):  
Karin P. Hammer ◽  
Julian Mustroph ◽  
Teresa Stauber ◽  
Walter Birchmeier ◽  
Stefan Wagner ◽  
...  

Arrhythmogenic right ventricular cardiomyopathy is a hereditary, rare disease with an increased risk for sudden cardiac death. The disease-causing mutations are located within the desmosomal complex and the highest incidence is found in plakophilin2. However, there are other factors playing a role for the disease progression unrelated to the genotype such as inflammation or exercise. Competitive sports have been identified as risk factor, but the type and extend of physical activity as cofactor for arrhythmogenesis remains under debate. We thus studied the effect of light voluntary exercise on cardiac health in a mouse model. Mice with a heterozygous PKP2 loss-of-function mutation were given the option to exercise in a running wheel which was monitored 24 h/d. We analyzed structural and functional development in vivo by echocardiography which revealed that neither the genotype nor the exercise caused any significant structural changes. Ejection fraction and fractional shortening were not influenced by the genotype itself, but exercise did cause a drop in both parameters after 8 weeks, which returned to normal after 16 weeks of training. The electrophysiological analysis revealed that the arrhythmogenic potential was slightly higher in heterozygous animals (50% vs 18% in wt littermates) and that an additional stressor (isoprenaline) did not lead to an increase of arrhythmogenic events pre run or after 8 weeks of running but the vulnerability was increased after 16 weeks. Exercise-induced alterations in Ca handling and contractility of isolated myocytes were mostly abolished in heterozygous animals. No fibrofatty replacements or rearrangement of gap junctions could be observed. Taken together we could show that light voluntary exercise can cause a transient aggravation of the mutation-induced phenotype which is abolished after long term exercise indicating a beneficial effect of long term light exercise.


2018 ◽  
Vol 4 (2) ◽  
pp. 99-117 ◽  
Author(s):  
Yang Yang ◽  
Ju Lu ◽  
Yi Zuo

Synaptic plasticity is widely believed to be the cellular basis of learning and memory. It is influenced by various factors including development, sensory experiences, and brain disorders. Long-term synaptic plasticity is accompanied by protein synthesis and trafficking, leading to structural changes of the synapse. In this review, we focus on the synaptic structural plasticity, which has mainly been studied with in vivo two-photon laser scanning microscopy. We also discuss how a special type of synapses, the multi-contact synapses (including those formed by multi-synaptic boutons and multi-synaptic spines), are associated with experience and learning.


2019 ◽  
Vol 30 (4) ◽  
pp. 2114-2127 ◽  
Author(s):  
E Vezzoli ◽  
C Calì ◽  
M De Roo ◽  
L Ponzoni ◽  
E Sogne ◽  
...  

Abstract Long-term memory formation (LTM) is a process accompanied by energy-demanding structural changes at synapses and increased spine density. Concomitant increases in both spine volume and postsynaptic density (PSD) surface area have been suggested but never quantified in vivo by clear-cut experimental evidence. Using novel object recognition in mice as a learning task followed by 3D electron microscopy analysis, we demonstrate that LTM induced all aforementioned synaptic changes, together with an increase in the size of astrocytic glycogen granules, which are a source of lactate for neurons. The selective inhibition of glycogen metabolism in astrocytes impaired learning, affecting all the related synaptic changes. Intrahippocampal administration of l-lactate rescued the behavioral phenotype, along with spine density within 24 hours. Spine dynamics in hippocampal organotypic slices undergoing theta burst-induced long-term potentiation was similarly affected by inhibition of glycogen metabolism and rescued by l-lactate. These results suggest that learning primes astrocytic energy stores and signaling to sustain synaptic plasticity via l-lactate.


Author(s):  
Alexander V Ruban ◽  
Sam Wilson

Abstract Non-photochemical chlorophyll fluorescence quenching (NPQ) remains one of the most studied topics of the 21st century in photosynthesis research. Over the past 30 years, profound knowledge has been obtained on the molecular mechanism of NPQ in higher plants. First, the largely overlooked significance of NPQ in protecting the reaction center of photosystem II (RCII) against damage, and the ways to assess its effectiveness are highlighted. Then, the key in vivo signals that can monitor the life of the major NPQ component, qE, are presented. Finally, recent knowledge on the site of qE and the possible molecular events that transmit ΔpH into the conformational change in the major LHCII [the major trimeric light harvesting complex of photosystem II (PSII)] antenna complex are discussed. Recently, number of reports on Arabidopsis mutants lacking various antenna components of PSII confirmed that the in vivo site of qE rests within the major trimeric LHCII complex. Experiments on biochemistry, spectroscopy, microscopy and molecular modeling suggest an interplay between thylakoid membrane geometry and the dynamics of LHCII, the PsbS (PSII subunit S) protein and thylakoid lipids. The molecular basis for the qE-related conformational change in the thylakoid membrane, including the possible onset of a hydrophobic mismatch between LHCII and lipids, potentiated by PsbS protein, begins to unfold.


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