An Acidic Exopolysaccharide fromHaloarcula hispanicaATCC33960 and Two Genes Responsible for Its Synthesis

A 1.1 × 106 Da acidic exopolysaccharide (EPS) was purified from an extremely halophilic archaeonHaloarcula hispanicaATCC33960 with a production of 30 mg L−1when grown in AS-168 medium, which mainly composed of mannose and galactose with a small amount of glucose in a molar ratio of 55.9 : 43.2 : 0.9. Two glycosyltransferase genes (HAH_1662andHAH_1667) were identified to be responsible for synthesis of the acidic EPS. Deletion of eitherHAH_1662orHAH_1667led to loss of the acidic EPS. The mutants displayed a different cell surface morphology, retarded growth in low salty environment, an increased adhesion, and swimming ability. Our results suggest that biosynthesis of the acidic EPS might act as an adaptable mechanism to protect the cells against harsh environments.

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Surface morphology and agglutination of lectin-treated human lymphocytes and lymphoblasts

Journal of Cell Science ◽

10.1242/jcs.21.3.563 ◽

1976 ◽

Vol 21 (3) ◽

pp. 563-578

Author(s):

J.H. Temmink ◽

J.G. Collard ◽

J. Roosien ◽

J.F. Van den Bosch

Keyword(s):

Cell Surface ◽

Surface Morphology ◽

Human Lymphocytes ◽

Cell Type ◽

A Cell ◽

Human Peripheral Lymphocytes ◽

Normal Human ◽

Altered Cell ◽

Induced Changes ◽

Cell Surface Morphology

Two human lymphoblasts (Raji and EB3) and normal human peripheral lymphocytes were exposed to different concentrations of Concanavalin A and wheat germ agglutinin. The lectin-induced agglutination was determined and correlated with lectin-induced changes in the surface morphology of these cells as studied in a scanning electron microscope. Whenever the lectin induced high agglutinability in a cell type, it also invariably had a smoothing effect on the cell surface. In contrast, when cells did not agglutinate well with a certain lectin, their cell surface remained essentially rough (villous) after addition of the lectin. The correlation found between increased agglutinability and altered cell surface morphology upon treatment with certain lectins suggests that both phenomena result from one and the same process. Additional evidence for this postulate is presented.

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Relationship of cell surface morphology and composition of Streptococcus salivarius K+ to adherence and hydrophobicity.

Infection and Immunity ◽

10.1128/iai.55.2.438-445.1987 ◽

1987 ◽

Vol 55 (2) ◽

pp. 438-445 ◽

Cited By ~ 17

Author(s):

A H Weerkamp ◽

H C van der Mei ◽

J W Slot

Keyword(s):

Cell Surface ◽

Surface Morphology ◽

Streptococcus Salivarius ◽

Relationship Of ◽

Cell Surface Morphology

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Differential inhibition of nerve growth factor and epidermal growth factor effects on the PC12 pheochromocytoma line.

The Journal of Cell Biology ◽

10.1083/jcb.98.2.417 ◽

1984 ◽

Vol 98 (2) ◽

pp. 417-426 ◽

Cited By ~ 72

Author(s):

P J Seeley ◽

A Rukenstein ◽

J L Connolly ◽

L A Greene

Keyword(s):

Nerve Growth Factor ◽

Growth Factor ◽

Epidermal Growth Factor ◽

Cell Surface ◽

Surface Morphology ◽

Neurite Outgrowth ◽

Decarboxylase Activity ◽

Differential Inhibition ◽

Epidermal Growth ◽

Cell Surface Morphology

Tests have been made of the action of the methyltransferase inhibitors 5'-S-methyl adenosine, 5'-S-(2-methyl-propyl)-adenosine, and 3-deaza-adenosine +/- L-homocysteine thiolactone, on nerve growth factor (NGF)-dependent events in the rat pheochromocytoma line PC12. Each of these agents inhibited NGF-dependent neurite outgrowth at concentrations of the order of millimolar. Slow initiation of neurite outgrowth over several days and more rapid regeneration of neurites (congruent to 1 d) were blocked, as was the priming mechanism necessary for genesis of neurites. The inhibitions were reversible in that PC12 cells maintained for several days in the presence of inhibitors grew neurites normally after washout of these agents. Other NGF-dependent responses of the PC12 line (i.e., induction of ornithine decarboxylase activity [over 4 h], enhancement of tyrosine hydroxylase phosphorylation [over 1 h], and rapid changes in cell surface morphology [30 s onward]) were inhibited by each of the agents. In contrast, corresponding epidermal growth factor-dependent responses in ornithine decarboxylase activity, phosphorylation, and cell surface morphology were not blocked, but instead either unaffected or enhanced, by the methylation inhibitors. These inhibitors did not act by blockade of binding of NGF to high- or low-affinity cell surface receptors, though they partially inhibited internalization of [125I]NGF. The inhibition of rapidly-induced NGF-dependent events and the differential inhibition of responses to NGF and epidermal growth factor imply that the methyltransferase inhibitors specifically block one of the first steps in the mechanistic pathway for NGF.

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