Intraperiplasmic Growth of Bdellovibrio bacteriovorus on Heat-Treated Escherichia coli

Abstract

Heat treatment (55°C for 40 min) of cell suspensions in buffer (ca. 3 x 109 cells per ml) of Escherichia coli ML35 caused a 4to 4.5-log loss of cell viability. Similar results were found for several other E. coli strains that were examined. As a result of this heat treatment, 260-nm-and 280-nm-absorbing materials were released into the suspending buffer, along with about 10% of the total cellular radioactivity, when cells uniformly labeled with 14C were used. In comparison with untreated cells, heat-treated E. coli ML35 cells showed (i) no significant changes in macromolecular composition other than ca. 22% less RNA content, (ii) an increased permeability to o-nitrophenyl-,8-D-galactopyranoside (a compound to which untreated cells are impermeable), (iii) almost complete loss of respiratory potential, and (iv) substantial losses of numerous glycolytic enzyme activities in cell extracts prepared from these cells. Intraperiplasmic development of Bdellovibrio bacteriovorus 109J with heat-treated E. coli ML35 as substrate cells appeared normal when observed microscopically, although bdellovibrio attachment and resultant bdelloplast formation were slightly retarded. No significant changes were observed in cell yields or in the ratios and contents of DNA, RNA, or protein between bdellovibrios harvested from untreated cells and those from heat-treated substrate cells after single-developmental-cycle growth on these cells. The average YATP values for intraperiplasmic growth on untreated and heattreated substrate cells were 16.0 and 17.9, respectively. It is concluded that intraperiplasmic bdellovibrio growth on gently heat-treated E. coli substrate cells is very similar to growth on untreated substrate cells, even though the former substrate cells are nonviable and substantially impaired in many metabolic activities.

Comparative biology of intracellular parasitism.

“…Here, the host is clearly passive and the parasite active. Bdellovibrios enter ultraviolet (UV)-killed (425) and heatkilled (183) hosts at undiminished rates, but anything that inhibits their motility (395,425) or their ability to synthesize protein (395) also inhibits attachment and entry. Just how the hole in the wall is made is not entirely certain.…”

Attachment of diaminopimelic acid to bdelloplast peptidoglycan during intraperiplasmic growth of Bdellovibrio bacteriovorus 109J

“…140 mCi/mmol, and from this value it was calculated that about 40,000 DAP residues were incorporated per bdelloplast. Based on the reported peptidoglycan content of E. coli ML35 (5 p.g/1010 cells [7]), this [3H]DAP (9 x 105 cpm/ml) to which either no additions (@) or 1(0), 3 (A), 10 (Fl), or 30 (A) nmoles of unlabeled carrier DAP per ml had been added. The amount of label appearing in TCA-insoluble material was determined during the growth cycle.…”

The Major Glycerophospholipids of the Predatory and Parasitic Bacterium Bdellovibrio bacteriovorus HID5

“…After collision and attachment to the surface the predator penetrates the host cell then proliferates in the intraperiplasmic space of the prey producing large, rounded bdelloplasts [7,8]. The parasitic phase is characterized by degradation of host macromolecules and uptake of the products into Bdellovibrio, which grows as a filament [9][10][11][12][13]. The filament forms septa and individual progeny cells are released during lysis of the host cell.…”