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Cell wall defects

Penicillins disrupt cell wall synthesis by inhibiting transpeptidase. When bacteria are in their growth and replication phase, penicillins are bactericidal due to cell wall defects, the bacteria swell and burst. [Pg.268]

A clearer indication of the stimulatory mechanism came from pretreatment studies. These were attempted on the premise that if these substances are used to repair a cell wall defect, it should be possible... [Pg.130]

Various core oligosaccharides have been isolated from the lipopolysaccharides of cell-wall-defective mutants of E. coli K-12 that are resistant to ampicillin. ... [Pg.253]

Cephalosporins affect the bacterial cell wall, making it defective and unstable This action is similar to the action of penicillin. The cephalosporins are usually bactericidal (capable of destroying bacteria). [Pg.75]

These circumstances became apparent to the authors when they attempted to study the formation of KDO 8-phosphate as catalyzed by purified bacterial extracts. These extracts did not catalyze the formation of KDO 8-phosphate from D-ribose 5-phosphate, but required D-arabinose 5-phosphate as the substrate Heath and Ghalambor29 showed that the KDO 8-phosphate synthetase reaction, observed in Pseudomonas extracts by Levin and Racker, is also catalyzed by extracts from Escherichia coli strains 0 111 B4 and J-5. Rick and Osborn136 showed that the KDO 8-phosphate synthetase from a Salmonella typhimurium mutant conditionally defective in cell-wall synthesis had a KM of 6 mM as compared to a KM of 170 pM for the enzyme from wild-type cells. [Pg.380]

Inpus erythematosus A chronic inflammatory disease of connective tissue, affecting the skin and internal organs, lymphoma A malignant tumor of the lymph nodes, multiple sclerosis A disease of the nervous system, myelodysplasia Abnormal or defective formation of the bone marrow. Mycoplasma Minute primitive bacteria without a rigid cell wall. Mycoplasma pneumoniae causes atypical pneumonia in humans, myeloma cells Malignant tumor cells. [Pg.443]

Another Arabidopsis mutant, murl, which lacks the ability to synthesize 1-fucose, possesses a defective gene encoding GDP-d-Man-4,6-dehydratase, a key enzyme in 1-fucose biosynthesis. Further analysis revealed that 1-Fuc is replaced by 1-Gal, a structurally similar monosaccharide, in the cell walls of this mutant with no adverse effects on plant physiology or metabolism (Rayon et al, 1999). Transgenic plants containing this mutation can also be used for foreign protein production. [Pg.106]

Localization of the enzyme in the periplasmic space is also consistent with the selective release of alkaline phosphatase during growth of an E. coli mutant which is osmotically sensitive because of a defective cell wall (14) and with the fact that phosphate esters which do not penetrate the protoplasmic membrane can be hydrolyzed by intact cells 15). In these latter measurements the activities found with intact cells as compared with equivalent cell extracts varied over wide limits depending upon the substrate and its concentration. This difference was assumed to result from a difference in the ease of penetration of the wall barrier by different phosphate esters. [Pg.375]

Shaver et al.40141 have shown that a considerable number of the initial microspheres are defective due to pores being eroded in the cell walls by oxidation during carbonization. The defective spheres are removed by sieving or by flotation fractionation, e.g. in acetone. [Pg.74]

The diameter of 24 A of the glass capillaries corresponds to the diameter of the water aggregates in the simple model of bulk water. From the point of this model one can assume that the strong interactions of the glass wall or the cell walls prevent the flickering process of the orientation defects. [Pg.158]

The ferroelectric hysteresis originates from the existence of irreversible polarization processes by polarization reversals of a single ferroelectric lattice cell (see Section 1.4.1). However, the exact interplay between this fundamental process, domain walls, defects and the overall appearance of the ferroelectric hysteresis is still not precisely known. The separation of the total polarization into reversible and irreversible contributions might facilitate the understanding of ferroelectric polarization mechanisms. Especially, the irreversible processes would be important for ferroelectric memory devices, since the reversible processes cannot be used to store information. [Pg.32]

Aside from the expression of histidine mutations that are easily detected, other properties have been built into the Salmonella strains by mutation to increase their sensitivity. The strains cure defective in DNA excision repair (uvrB). In this case, the increased sensitivity probably is due to the failure to remove some DNA adducts that could lead to mutation. The strains also possess a mutation (rfa) that removes part of the lipopolysaccharide barrier of the bacterial cell wall and thereby makes the cells more permeable to some chemicals. Finally, Salmonella strains TA98 and TA100 contain the R-factor plasmid pkMIOl,277 which increases sensitivity probably by increasing the activity of an error-prone DNA-repair system. [Pg.85]

Since we have been unable to detect changes in other cell fractions which correlate with improvements in accumulation capacity, it appears reasonable to conclude, especially in view of the previously cited osmotic evidence, that a lack in cell wall rigidity limits the accumulation capacity of LB6 cells and that the repair of the wall defect suffices to permit these cells to express normal accumulation capacity. On the question of the participation of vitamin B6 in amino acid transport, these, and especially the osmotic experiments, are clearly inconsistent with the suggested catalytic role of this substance directly in the entry reaction. [Pg.132]

Therefore, the three vitamin deficiencies so far studied in detail appear to affect amino acid transport and accumulation in similar but indirect ways. The accumulation defect is most pronounced in vitamin B6-deficient cells, for which there is also strong evidence implicating an abnormality in cell wall composition as a likely source of the change in transport activity. Direct evidence for a cell wall change in biotin- and pantothenate-deficient cells has not yet been obtained. The possibility remains, therefore, that the change in accumulation activity may be caused by an abnormality in some other structural component such as the peripheral cell membrane. [Pg.134]


See other pages where Cell wall defects is mentioned: [Pg.191]    [Pg.270]    [Pg.148]    [Pg.313]    [Pg.123]    [Pg.447]    [Pg.191]    [Pg.270]    [Pg.148]    [Pg.313]    [Pg.123]    [Pg.447]    [Pg.482]    [Pg.536]    [Pg.167]    [Pg.77]    [Pg.80]    [Pg.108]    [Pg.311]    [Pg.237]    [Pg.84]    [Pg.260]    [Pg.1516]    [Pg.400]    [Pg.21]    [Pg.602]    [Pg.19]    [Pg.20]    [Pg.107]    [Pg.117]    [Pg.715]    [Pg.158]    [Pg.220]    [Pg.449]    [Pg.456]    [Pg.54]    [Pg.103]    [Pg.190]    [Pg.125]    [Pg.102]   
See also in sourсe #XX -- [ Pg.191 ]




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Defects walls

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