In:
Proceedings of the National Academy of Sciences, Proceedings of the National Academy of Sciences, Vol. 80, No. 2 ( 1983-01), p. 579-583
Abstract:
We have studied the physiological effects of mitomycin C induction on cells carrying ColE1 plasmids with differing configurations of three genes: the structural gene coding for colicin ( cea ), a gene responsible for mitomycin C lethality ( kil ) that we located as part of an operon with cea , and the immunity ( imm ) gene, which lies near cea but is not in the same operon. kil is close to or overlaps imm . When cea + plasmids are present mitomycin C induction results in 100-fold or greater increases in the level of colicin. Within an hour after induction more than 90% of cells carrying cea + kil + plasmids are killed and macromolecular synthesis stops, capacity for transport of proline, thiomethyl β-D-galactoside, and α-methyl glucoside is lost, and the membrane becomes abnormally permeable as indicated by an increased accessibility of intracellular β-galactosidase to the substrate o -nitrophenyl β-D-galactoside. All of these events occur when a cea - kil + imm + plasmid is present and none does when the plasmid is cea + kil - imm + , so the damage can be attributed solely to the Kil function and not to the presence of colicin. However, cells carrying a cea + kil - imm - plasmid are killed upon induction, apparently by action of endogenous colicin on the nonimmune cytoplasmic membrane. The pattern of accompanying physiological damage is distinguished from the kil + -associated damage by an enhancement of α-methyl glucoside uptake and accumulation and efflux of α-methyl glucoside 6-phosphate and by an absence of the alteration in membrane permeability for o -nitrophenyl β-D-galactoside. These features are typical of colicin E1 action on the membrane. The induced damage is not prevented by trypsin and occurs in cells of a strain specifically tolerant to exogenous colicin E1, indicating that the attack is from inside the cell.
Type of Medium:
Online Resource
ISSN:
0027-8424
,
1091-6490
DOI:
10.1073/pnas.80.2.579
Language:
English
Publisher:
Proceedings of the National Academy of Sciences
Publication Date:
1983
detail.hit.zdb_id:
209104-5
detail.hit.zdb_id:
1461794-8
SSG:
11
SSG:
12
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