1973Canadian Journal of MicrobiologyRequires access

Influence of cell-wall thickness on cell division: electron microscopic study with Bacillus cereus

K. L. Chung

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Abstract

Bacillus cereus that had been exposed to chloramphenicol for 0 and 90 min synthesized walls whose thickness increased with time. These cells were washed and resuspended in fresh growth medium. Cell division was examined by electron microscopy. In untreated cells, a slight invagination of the cytoplasmic membrane with deposit of cross-wall material marked the onset of cell division. The cross wall grew inward until the septum was about [Formula: see text] completed. This was followed by splitting and bifurcation of the outer edge of the cross wall, which in turn separated the peripheral wall scars. Cross-wall penetration with further splitting continued until the daughter cells were completely partitioned. The peripheral wall scars that were located at the junction of peripheral and end walls at the time of cell separation indicated that the zone of cell division was probably not a region of active cell elongation. In cells treated with chloramphenicol for 90 min, cross-wall initiation and completion all occurred beneath a thickened peripheral wall. The circumferential portion of the peripheral wall at the zone of cell division appeared to be responsible for the hindrance of cell separation. This thick layer subsequently severed at three or four sites to allow the separation of daughter cells. For cells that had initiated cross-wall invagination at the time when chloramphenicol was added, accumulation of a large amount of cross-wall material at the zone of cell division was observed. Upon removal of the antibiotic, cells abandoned the old and initiated a new dividing site. For cells that had already completed cross-wall formation at the time of chloramphenicol treatment, the increase in wall thickness did not appear to interfere with cell separation. Models for the different stages of cell division in all these bacteria were presented.

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Bacillus cereus that had been exposed to chloramphenicol for 0 and 90 min synthesized walls whose thickness increased with time. These cells were washed and resuspended in fresh growth medium. Cell division was examined by electron microscopy. In untreated cells, a slight invagination of the cytoplasmic membrane with deposit of cross-wall material marked the onset of cell division. The cross wall grew inward until the septum was about [Formula: see text] completed. This was followed by splitting and bifurcation of the outer edge of the cross wall, which in turn separated the peripheral wall scars. Cross-wall penetration with further splitting continued until the daughter cells were completely partitioned. The peripheral wall scars that were located at the junction of peripheral and end walls at the time of cell separation indicated that the zone of cell division was probably not a region of active cell elongation. In cells treated with chloramphenicol for 90 min, cross-wall initiation and completion all occurred beneath a thickened peripheral wall. The circumferential portion of the peripheral wall at the zone of cell division appeared to be responsible for the hindrance of cell separation. This thick layer subsequently severed at three or four sites to allow the separation of daughter cells. For cells that had initiated cross-wall invagination at the time when chloramphenicol was added, accumulation of a large amount of cross-wall material at the zone of cell division was observed. Upon removal of the antibiotic, cells abandoned the old and initiated a new dividing site. For cells that had already completed cross-wall formation at the time of chloramphenicol treatment, the increase in wall thickness did not appear to interfere with cell separation. Models for the different stages of cell division in all these bacteria were presented.

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Available abstract

Bacillus cereus that had been exposed to chloramphenicol for 0 and 90 min synthesized walls whose thickness increased with time. These cells were washed and resuspended in fresh growth medium. Cell division was examined by electron microscopy. In untreated cells, a slight invagination of the cytoplasmic membrane with deposit of cross-wall material marked the onset of cell division. The cross wall grew inward until the septum was about [Formula: see text] completed. This was followed by splitting and bifurcation of the outer edge of the cross wall, which in turn separated the peripheral wall scars. Cross-wall penetration with further splitting continued until the daughter cells were completely partitioned. The peripheral wall scars that were located at the junction of peripheral and end walls at the time of cell separation indicated that the zone of cell division was probably not a region of active cell elongation. In cells treated with chloramphenicol for 90 min, cross-wall initiation and completion all occurred beneath a thickened peripheral wall. The circumferential portion of the peripheral wall at the zone of cell division appeared to be responsible for the hindrance of cell separation. This thick layer subsequently severed at three or four sites to allow the separation of daughter cells. For cells that had initiated cross-wall invagination at the time when chloramphenicol was added, accumulation of a large amount of cross-wall material at the zone of cell division was observed. Upon removal of the antibiotic, cells abandoned the old and initiated a new dividing site. For cells that had already completed cross-wall formation at the time of chloramphenicol treatment, the increase in wall thickness did not appear to interfere with cell separation. Models for the different stages of cell division in all these bacteria were presented.

Key concepts: Cell wall, Cell division, Elongation, Cytoplasm, Biophysics, Chloramphenicol, Cytokinesis, Bacillus cereus

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