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FINE STRUCTURAL CHANGES IN RESPONSE TO HORMONAL STIMULATION OF THE PERFUSED CANINE PANCREAS.

The dog pancreas isolated in situ was perfused with oxygenated dog blood and stimulated with pancreozymin, secretin, or both. There were no significant changes in the fine structure of the acinar, centroacinar, or duct cells attributable to the perfusion. Combined glutaraldehyde and osmium fixation gave good preservation of the secretory products of the acinar cell. Before stimulation, the lumen of the acini is filled with material similar in texture to the content of the zymogen granules, but of somewhat lower density. Release of secretion commonly takes place by coalescence of the limiting membrane of zymogen granules with the plasmalemma, but one granule opening at the surface may frequently be joined by others coalescing with its membrane and forming an interconnected series all with contents having the same texture as the released zymogen. Such a mechanism seems to permit a more rapid release of secretory product than discharge of individual granules. Pancreozymin stimulation caused marked depletion of zymogen granules, but no obvious changes in the Golgi apparatus. It is clear, therefore, that this hormone exerts its effect upon release of granules rather than upon their formation. Secretin stimulation of water and bicarbonate secretion caused a marked washing out of the luminal contents, but had little detectable effect on cellular structure.

Animals↗

Dynamics of protein and chromophore structural changes in the photocycle of photoactive yellow protein monitored by time-resolved optical rotatory dispersion.

The dynamics of the PYP photocycle have been studied using time-resolved optical rotatory dispersion (TRORD) spectroscopy in the visible and far-UV spectral regions to probe the changes in the chromophore configuration and the protein secondary structure, respectively. The changes in the secondary structure in PYP upon photoisomerization of the chromophore can be described by two exponential lifetimes of 2 +/- 0.8 and 650 +/- 100 ms that correspond to unfolding and refolding processes, respectively. The TRORD experiments that follow the dynamics of the chromophore report three exponential components, with lifetimes of 10 +/- 3 micros, 1.5 +/- 0.5 ms, and 515 +/- 110 ms. A comparison of the kinetic behaviors of the chromophore and protein shows that during the decay of pR(465) an initial relaxation that is localized to the chromophore hydrophobic pocket precedes the formation of the chromophore and protein structures found in pB(355). In contrast, the protein and chromophore processes occur with similar time constants during inactivation of the signaling state.

Bacterial Proteins↗

Hypertensive structural changes in systemic precapillary resistance vessels: how important are they for in vivo haemodynamics?

OBJECTIVE: To discuss recent findings that seem to question the importance of structural vascular changes for the raised resistance observed in hypertension. MAIN ISSUES: First, in daily life situations, the proximal resistance sections, which are the main site for vasoconstrictor fibre effects, are also the main site for structural elevation of resistance in hypertension. The most distal ones are crucially important for local flow distribution, and their unaltered design suggests that they are usually protected from pressure elevations by a raised resistance upstream. Furthermore, recent findings indicate that central neurohormonal mechanisms are much more important than myogenic ones for inducing hypertension at least in spontaneously hypertensive rats. Second, the function of structurally altered resistance vessels is often misunderstood, mainly because the haemodynamic importance of wall distensibility is disregarded. Vascular geometric design and distensibility tend to be altered to an 'ideal' extent, so that with ordinary changes in smooth muscle activity a normal flow range is maintained, despite elevations in both perfusion and transmural pressures and in resistance. Third, the rapid normalization of blood pressure on declipping of two-kidney, one clip or of one-kidney, one clip renally hypertensive rats by no means refutes the haemodynamic importance of a prevailing structural upward resetting. Declipping leads to a powerful and prolonged release of vasodilator-sympathoinhibitory medullipins, which create a subnormal smooth muscle tone. Because the structurally hyper-reactive resistance vessels now operate along a steeper resistance curve the pressure fall becomes, if anything, accentuated, which opens the way for structural regression. Fourth, the highly sophisticated and often differentiated neurohormonal control system usually explains why vasoactive agents, for example, do not regularly produce exaggerated pressure changes in vivo, even in the presence of hypertensive structural changes. In addition, counteracting effects by endothelial mechanosensitive mechanisms seem to be of great importance in these situations. CONCLUSION: The arguments and views outlined recently do not, on closer scrutiny and for the reasons given, really challenge the importance of structural vascular changes in hypertension in vivo and may, indeed, in some respects serve to support this concept.

Animals↗

Redox-dependent structural changes in an engineered heme-copper center in myoglobin: insights into chloride binding to CuB in heme copper oxidases.

The effects of chloride on the redox properties of an engineered binuclear heme-copper center in myoglobin (Cu(B)Mb) were studied by UV-vis spectroelectrochemistry and EPR spectroscopy. A low-spin heme Fe(III)-Cu(I) intermediate was observed during the redox titration of Cu(B)Mb only in the presence of both Cu(II) and chloride. Upon the first electron transfer to the Cu(B) center, one of the His ligands of Cu(B) center dissociates and coordinates to the heme iron, forming a six-coordinate low-spin ferric heme center and a reduced Cu(B) center. The second electron transfer reduces the ferric heme and causes the release of the coordinated His ligand. Thus, the fully reduced state of the heme-copper center contains a five-coordinate ferrous heme and a reduced Cu(B) center, ready for O(2) binding and reduction to water to occur. In the absence of a chloride ion, formation of the low-spin heme species was not observed. These redox reactions are completely reversible. These results indicate that binding of chloride to the Cu(B) center can induce redox-dependent structural changes, and the bound chloride and hydroxide in the heme-copper center may play different roles in the redox-linked enzymatic reactions of heme-copper oxidases, probably because of their different binding affinity to the copper center and the relatively high concentration of chloride under physiological conditions.

Amino Acid Substitution↗

Regulation of mouse mammary tumor virus env transcriptional activator initiated mammary tumor virus superantigen transcripts in lymphomas of SJL/J mice: role of Ikaros, demethylation, and chromatin structural change in the transcriptional activation of mammary tumor virus superantigen.

Mammary tumor virus (Mtv29)-encoded superantigen expressed by SJL/J mouse B cell lymphomas stimulates CD4+V16+ T cells and thereby acquires T cell help necessary for lymphoma growth. Mtv29 mouse mammary tumor virus env transcriptional activator (META) env-controlled Mtv29 superantigen (vSAg29) mRNA transcripts (1.8 kb) are not expressed in normal B or other somatic cells. Real-time PCR-based assays with DNA from normal SJL liver and vSAg29- lymphoma (cNJ101), digested with methylation-sensitive enzymes, showed hypermethylation at AvaI, FspI, HpaII, ThaI, and the distal HgaI sites of the META env, but vSAg29+ lymphoma cells showed significant demethylation at AvaI, HpaII, and the distal HgaI sites. The distal HgaI site that is adjacent to an Ikaros binding site is significantly demethylated in the META env DNA from primary lymphomas. Gel shift assays showed binding of Ikaros to a sequence representing this region in the META env. SJL lymphomas expressed the Ikaros isoform Ik6 that was absent in normal B cells. vSAg29+ cells exhibited increased DNaseI accessibility to chromatin at the vSAg29 initiation site. Treatment of cNJ101 cells with a demethylating agent, 5-azacytidine, and a histone deacetylase inhibitor, trichostatin A, caused hypomethylation at AvaI, HpaII, and distal HgaI sites and led to chromatin structural change at the vSAg29 initiation site, accompanied by the expression of vSAg29 transcripts. This enabled cNJ101 cells to stimulate SJL lymphoma-responsive CD4+V16+ T hybridoma cells. Thus, demethylation at the distal HgaI site of the Mtv29 META env permits vSAg29 expression, which may have an impact on the development of germinal center-derived B cell lymphomas of SJL/J mice.

Animals↗

Sequential structural changes of Escherichia coli thioesterase/protease I in the serial formation of Michaelis and tetrahedral complexes with diethyl p-nitrophenyl phosphate.

Escherichia coli thioesterase/protease I (TEP-I) belongs to a new subclass of lipolytic enzymes of the serine hydrolase superfamily. Here we report the first direct NMR observation of the formation of the Michaelis complex (MC) between TEP-I and diethyl p-nitrophenyl phosphate (DENP), an active site directed inhibitor of serine protease, and its subsequent conversion to the tetrahedral complex (TC). NMR, ESI-MS, and kinetic data showed that DENP binds to TEP-I in a two-step process, a fast formation of MC followed by a slow conversion to TC. NMR chemical shift perturbation further revealed that perturbations were confined mainly to four conserved segments comprising the active site. Comparable magnitudes of chemical shift perturbations were detected in both steps. The largest chemical shift perturbation occurred around the catalytic Ser(10). In MC, the conformation of the mobile Ser(10) was stabilized, and its amide resonance became observable. From the large chemical shift perturbation upon conversion from MC to TC, we propose that the amide protons of Ser(10) and Gly(44) serve as the oxyanion hole proton donors that stabilize the tetrahedral adduct. The pattern of residues perturbed in both steps suggests a sequential, stepwise structural change upon binding of DENP. The present study also demonstrates the important catalytic roles of conserved residues in the SGNH family of proteins.

Binding Sites↗

Evidence of a calcium-induced structural change in the ATP-binding site of the sarcoplasmic-reticulum Ca2+-ATPase using terbium formycin triphosphate as an analogue of Mg-ATP.

Terbium ions and terbium formycin triphosphate have been used to investigate the interactions between the cation and nucleotide binding sites of the sarcoplasmic reticulum Ca2+-ATPase. Three classes of Tb3+-binding sites have been found: a first class of low-affinity (Kd = 10 microM) corresponds to magnesium binding sites, located near a tryptophan residue of the protein; a second class of much higher affinity (less than 0.1 microM) corresponds to the calcium transport sites, their occupancy by terbium induces the E1 to E2 conformational change of the Ca2+-ATPase; a third class of sites is revealed by following the fluorescence transfer from formycin triphosphate (FTP) to terbium, evidencing that terbium ions can also bind into the nucleotide binding site at the same time as FTP. Substitution of H2O by D2O shows that Tb-FTP binding to the enzyme nucleotide site is associated with an important dehydration of the terbium ions associated with FTP. Two terbium ions, at least, bind to the Ca2+-ATPase in the close vicinity of FTP when this nucleotide is bound to the ATPase nucleotide site. Addition of calcium quenches the fluorescence signal of the terbium-FTP complex bound to the enzyme. Calcium concentration dependence shows that this effect is associated with the replacement of terbium by calcium in the transport sites, inducing the E2----E1 transconformation when calcium is bound. One interpretation of this fluorescence quenching is that the E1----E2 transition induces an important structural change in the nucleotide site. Another interpretation is that the high-affinity calcium sites are located very close to the Tb-FTP complex bound to the nucleotide site.

Adenosine Triphosphate↗

An X-ray solution scattering study of the cofactor and activator induced structural changes in yeast pyruvate decarboxylase (PDC).

Structure and activation pattern of pyruvate decarboxylase (PDC) from yeast was studied by synchrotron radiation X-ray solution scattering. The results give a direct proof that the reversible deactivation of PDC at pH 8.0 is accompanied by the dissociation of the tetrameric holoenzyme into dimeric halves. The kinetics of this process was followed. At pH 6.5 the dimeric halves reassociate to a tetramer even in the absence of cofactors. The changes of the scattering pattern upon binding of the substrate-like activator pyruvamide indicate that the structure expands in the course of the enzyme activation.

Apoenzymes↗

Indirect evidence for structural changes coupled with QB-. formation in photosystem II.

The thermal blockage of QA-. oxidation was analysed in PS II membrane fragments by monitoring flash-induced changes of the relative fluorescence quantum yield as a function of temperature. The results obtained reveal: (a) in dark-adapted samples the fraction of QA-. that is not reoxidised within a time domain of 10 s after the actinic flash increases with lowering the temperature (half-maximum effect at 250-260 K), (b) at low temperatures where QA-. generated in dark-adapted samples remains almost completely reduced, a significant extent of QA-. reoxidation arises when samples are used that were preilluminated at room temperature by one saturating flash followed by rapid freezing before performing the experiment, and (c) the extent of QA-. that is reoxidised at 258 K exhibits a characteristic binary oscillation as a function of the number of preillumination flashes given at room temperature. Based on these data it is inferred that QB and QB-. are located at different equilibrium positions in the QB site. As a consequence the formation of QB-. is coupled with significant structural changes that require sufficient flexibility of the protein matrix. This general feature corresponds with a recently proposed model for the acceptor side reactions of anoxygenic bacteria [Stowell, M.H.B., McPhillips, T.M., Rees, D.C., Soltis, S.M., Abresch, E. and Feher, G., Science 276 (1997) 812-816].

Darkness↗

Coupled structure changes of SecA and SecG revealed by the synthetic lethality of the secAcsR11 and delta secG::kan double mutant.

An Escherichia coli strain carrying either the secAcsR11 or delta secG::kan mutation is unable to grow at low temperature owing to cold-sensitive protein translocation but grows normally at 37 degree C. However, introduction of the two mutations into the same cells caused a severe defect in protein translocation and the cells were unable to grow at any temperature examined, indicating that secG is essential for the secAcsR11 mutant. The mutant SecA (csSecA) was found to possess a single amino acid substitution in the precursor-binding region and was defective in the interaction with the precursor protein. Furthermore, the membrane insertion of SecA and the membrane topology inversion of SecG, both of which took place upon the initiation of protein translocation, were significantly retarded even at 37 degree C, when csSecA was used instead of the wild-type SecA. The insertion of the wild-type SecA was also significantly defective when SecG-depleted membrane vesicles were used in place of SecG-containing ones. No insertion of csSecA occurred into SecG-depleted membrane vesicles. Examination of in vitro protein translocation at 37 degree C revealed that SecG is essential for csSecA-dependent protein translocation. We conclude that SecG and SecA undergo a coupled structure change, that is critical for efficient protein translocation.

Adenosine Triphosphatases↗

Administration of antenatal glucocorticoids prevents pulmonary artery structural changes in nitrofen-induced congenital diaphragmatic hernia in rats.

BACKGROUND/PURPOSE: The aim of this study was to investigate whether maternal administration of dexamethasone has any effect on pulmonary vasculature in nitrofen-induced experimental congenital diaphragmatic hernia (CDH) in a rat model. METHODS: A CDH model was induced in pregnant rats after administration of 100 mg nitrofen on day 9.5 of gestation. Antenatal dexamethasone, 0.25 mg/kg was given intraperitoneally on day 18.5 and 19.5 of gestation. The fetuses were divided into three groups: group I (n = 10), normal controls; group II (n = 10), nitrofen-induced CDH; group III (n = 10), nitrofen-induced CDH with maternal antenatal dexamethasone treatment. The fetuses were killed by cesarean section at term. Victorian blue van Gieson staining and immunostaining with antialpha smooth muscle actin (ASMA) were performed on lung tissue. The degree of adventitial thickness and area, and medial thickness and area were measured in pulmonary arteries by image analyzer and analyzed statistically. RESULTS: There was a significant increase in adventitial thickness and area in group II compared with group I and III (P < .01). There was also a significant increase in medial thickness in group II compared with group I and III (P < .01). The degree of adventitial thickness and area and degree of medial thickness and area were similar in controls and maternal dexamethasone-treated CDH group. CONCLUSION: This study demonstrates that antenatal maternal dexamethasone treatment prevents pulmonary artery structural changes in nitrofen-induced CDH in rats.

Animals↗

Phosphorylation of multiple CD3 zeta tyrosine residues leads to formation of pp21 in vitro and in vivo. Structural changes upon T cell receptor stimulation.

T lymphocyte activation resulting from antigen recognition involves a protein tyrosine kinase pathway which triggers phosphorylation of several cellular substrates including the CD3 zeta subunit of the T cell receptor (TCR) to form pp21. The homologous TCR-associated protein, CD3 eta, is an alternatively spliced product of the same gene locus as CD3 zeta. CD3 eta lacks one of six cytoplasmic tyrosine residues (Tyr-132) found in CD3 zeta and is itself not phosphorylated. Site-directed mutagenesis in conjunction with in vitro and in vivo phosphorylation studies herein demonstrates that Tyr-132 is required for the formation of pp21. Moreover, the differential phosphorylation of CD3 zeta versus CD3 eta is not due to a selective association of the known TCR-associated protein tyrosine kinase, p59fyn; p59fyn but not p56lck or p62yes is associated with each of the three TCR isoforms containing CD3 zeta 2, or CD3 eta 2, or CD3 zeta-eta. This association occurs through components of the TCR complex distinct from CD3 zeta or CD3 eta. In addition, we show that pp21 formation is not only dependent on Tyr-132 but results from concomitant phosphorylation of other CD3 zeta residues including Tyr-121. Mutation of Tyr-90, -121, or -132 does not alter primary signal transduction as shown by the ability of individual CD3 zeta Tyr----Phe mutants to produce interleukin-2 upon TCR stimulation. Thus, the substantial structural changes in CD3 zeta upon TCR stimulation as reflected by alteration in its mobility in sodium dodecyl sulfate-polyacrylamide gel electrophoresis may affect subsequent events such as receptor desensitization, receptor movement, and/or protein associations.

Amino Acid Sequence↗

[Redifferentiation and a karyotypic structural change in populations of tumorous rhabdomyoblasts proliferating in the anterior chamber of the eye].

A study was made of the transplantable rhabdomyosarcoma of mice M-62 during its transplantation after 15 passages simultaneously into the subcutaneous connective tissue and the eye anterior chamber (EAC), the latter being an immunologically advantageous site. The transplantable rhabdomyosarcoma cell populations, proliferating in EAC, are characterized by a higher differentiation level as compared with those proliferating in the subcutaneous connective tissue, the cells being taken from the same tumour, at the same passage. Morphologically it is expressed in the appearance of cytotypical (myofibrils in mononuclear tumour myoblasts) and histotypical (formation of myosymplasts) characters of differentiation. The increase in the intensity of differentiation correlates with changes in the ratios of M- and H-forms of LDH towards that which is characteristic of the definitive skeletal muscle tissue. A more intensive differentiation occurs on the background of changes in the karyotype structure of the populations of tumour myoblasts expressed in the increased share of diploid cells. An assumptions is made that the populations of tumour cells proliferating in EAC, i. e. under conditions of isolation from the immunological reactions of the organism, demonstrate changes towards normalization.

Animals↗

Sequential structural changes upon zinc and calcium binding to metal-free concanavalin A.

The lectin concanavalin A (ConA) sequentially binds a transition metal ion in the metal-binding site S1 and a calcium ion in the metal-binding site S2 to form its saccharide-binding site. Metal-free ConA crystals soaked with either Zn2+ (apoZn-ConA) or Co2+ (apoCo-ConA) display partial binding of these ions in the proto-transition metal-binding site, but no further conformational changes are observed. These structures can represent the very first step in going from metal-free ConA toward the holoprotein. In the co-crystals of metal-free ConA with Zn2+ (Zn-ConA), the zinc ion can fully occupy the S1 site. The positions of the carboxylate ligands Asp10 and Asp19 that bridge the S1 and S2 sites are affected. The ligation to Zn2+ orients Asp10 optimally for calcium ligation and stabilizes Asp19 by a hydrogen bond to one of its water ligands. The neutralizing and stabilizing effect of the binding of Zn2+ in S1 is necessary to allow for subsequent Ca2+ binding in the S2 site. However, the S2 site of monometallized ConA is still disrupted. The co-crystals of metal-free ConA with both Zn2+ and Ca2+ contain the active holoprotein (ConA ZnCa). Ca2+ has induced large conformational changes to stabilize its hepta-coordination in the S2 site, which comprise the trans to cis isomerization of the Ala207-Asp208 peptide bond accompanied by the formation of the saccharide-binding site. The Zn2+ ligation in ConA ZnCa is similar to Mn2+, Cd2+, Co2+, or Ni2+ ligation in the S1 site, in disagreement with earlier extended x-ray absorption fine structure results that suggested a lower coordination number for Zn2+.

Amino Acid Sequence↗

Adolescent smokers and nonsmokers: profiles and their changing structure.

The status of smoking among tenth-graders in Jerusalem high schools as part of a smoking prevention program was examined. Two consecutive cohorts of 792 and 771 subjects were given questionnaires on two occasions: at the onset of the study (fall 1980 for the first cohort and fall 1981 for the second), and either 2 years (first cohort) or 1 year (second cohort) later. Based on the theory that smoking relates to counterconformity entailing rebelliousness and conformity to a nonconformist peer culture, subjects were asked about their behaviors and cognitions concerning school, home, peers, drinking, and smoking. It was reasoned that no single variable can predict, let alone explain, the onset and continuation of smoking and that the various factors that relate to smoking and distinguish between smokers and nonsmokers (a) constitute a systematic and coherent syndrome of counterconformity variables, which (b) reinforce each other, and (c) that over time, smoking and counterconformity come to affect each other reciprocally. These hypotheses were supported by the data. Smokers were found to differ from nonsmokers in a number of ways that were all related to counterconformity. Truancy and an inability to resist peer pressure to smoke, manifestations of two aspects of this syndrome, were the best predictors of smoking for both sexes, both cohorts, and both measuring occasions. With time, personal rebelliousness tended to become a weaker predictor, while social interaction variables became relatively stronger. The intercorrelations among the nonsmokers who became smokers were the highest, as predicted. The nature of the syndrome, its changing structure, and implications for prevention are discussed.

Achievement↗

Does cytosolic free calcium concentration in platelets reflect tone and structural changes of resistance vessels?

To investigate tone and vascular changes of resistance vessels as related to cytosolic free calcium concentration [( Ca2+]i) in platelets, we measured forearm vascular resistance and free calcium concentration in platelets from 10 essential hypertensives and 15 normotensives. The [Ca2+]i in platelets was significantly higher in essential hypertensives than in normotensives (184 +/- 43 versus 146 +/- 23 nmol/l, P less than 0.01). The [Ca2+]i levels in platelets were significantly correlated with both systolic (r = 0.50, P less than 0.05) and diastolic blood pressures (r = 0.57, P less than 0.01). Resting vascular resistance and minimal vascular resistance were significantly higher in essential hypertensives than in normotensives (30.6 +/- 12.6 and 2.57 +/- 1.30 versus 16.3 +/- 8.0 and 1.47 +/- 0.63 mmHg/ml per min per 100 ml, P less than 0.05 and P less than 0.01, respectively). Both resting and minimal vascular resistance were significantly correlated with [Ca2+]i in platelets (r = 0.40 and P less than 0.05, r = 0.55 and P less than 0.01, respectively). These results suggest that [Ca2+]i in platelets reflects [Ca2+]i in vascular smooth muscle cells and may be a significant determinant of not only tone but also structural changes of resistance vessels.

Adult↗

Pulmonary artery structural changes in pulmonary hypertension complicating congenital diaphragmatic hernia.

Primary pulmonary hypertension is characterized by the presence of smooth muscle cells in nonmuscular compartments or segments of the vessel and the abnormal deposition of collagen in both the small muscular arteries and arterioles and the large elastic arteries. Victorian blue van Gieson staining and Immunostaining with anti-alpha smooth muscle actin (ASMA) were performed on lung tissues obtained during autopsy from 21 patients who had congenital diaphragmatic hernia (CDH) complicated by persistent pulmonary hypertension (PPH) and 10 control patients who died of sudden infant death syndrome (SIDS). The degree of medial thickening and adventitial thickening was measured in pulmonary arteries by image analysis and compared statistically. There was a significant increase in adventitial as well as medial thickness in arteries of all sizes in CDH patients compared with control patients (P < .001). The most striking increase occurred in arteries with an external diameter (ED) of less than 75 microns. Calculation of the areas of the various components in the wall of each vessel showed that for smaller vessels (< 75 microns ED), the area of the lumen was smaller and the area of the media and adventitia was larger in CDH patients compared with control patients (P < < .001). In vessels greater than 75 microns ED, the areas of media in CDH was the same as in controls and the area of adventitia in CDH was significantly larger than controls (P < .001). The present study provides evidence that an increase in adventitial thickness and adventitial area occurs in pulmonary arteries in CDH patients complicated by PPH. The structural changes in the adventitia of the pulmonary arteries may be an important factor in the development of PPH in patients with CDH.

Actins↗

[Structural changes of chloroplasts and galactolipid contents in Chlorella cells during clinorotation].

Research of chloroplast ultrastructure in Chlorella cells grown during long-term period under clinorotation has been carried out. Different changes of the chloroplast structure, concerning both the amount of starch grains and stroma electron density as well as membrane system have been revealed. Occurrence of more significant bends of the thylakoids compared to the control and more loose arrangement of the thylakoids in a bunch were noted. The most significant changes were observed in a membrane system, in particular, appearance of the non-uniform expansions of the inter- and intrathylakoid spaces in Chlorella chloroplasts. Taking into account the role of galactolipids as important components of the photosynthetic membranes, the content of general galactolipids, monogalactosyldiacylglycerol and digalactosyldiacylglicerol in Chlorella cells was determined. It was assumed that statistically significant increase of the galactolipid content, especially of MDG, can probably be one of the reasons of membrane system reorganizations in Chlorella cells under altered gravity.

Chlorella↗