noninherited resistance

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" Balaban et al. investigated the growth dynamics of various mutant and

wild-type Escherichia coli using a microfluidic device to track

individual organisms. At least three different phenotypes were

revealed. Those with a normal growth rate were killed. Type I

persisters exited stationary phase very slowly--hours rather than

minutes after nutrients were restored. Type II persisters arose by a

spontaneous switch from the normal growth rate to grow consistently

more slowly, regardless of growth conditions, and, rarely, could

switch back to the normal growth rate. "

" et al. (see the Perspective by Levin) describe another

mechanism for avoiding the lethal effects of antibiotics. Damage to

penicillin binding protein 3 activates the DpiBA two-component signal

transduction cascade and eventually triggers the SOS DNA repair

response. When SOS kicks in, cell division pauses, and the bacteria

escape lethal damage, at least from short-term antibiotic exposure,

because synthesis of new cell walls shuts down. "

quote from Bacterial Persistence and Antibiotic Resistance. Sci. STKE

2004, tw331 (2004).

refs:

N. Q. Balaban, J. Merrin, R. Chait, L. Kowalik, S. Leibler, Bacterial

persistence as a phenotypic switch. Science 305, 1622-1625 (2004).

[Abstract] [Full Text]

B. R. Levin, Noninherited resistance to antibiotics. Science 305,

1578-1579 (2004). [summary] [Full Text]

C. , L. E. Thomsen, C. Gaggero, R. Mosseri, H. Ingmer, S. N.

Cohen, SOS response induction by ß-lactams and bacterial defense

against antibiotic lethality. Science 305, 1629-1631 (2004).

[Abstract] [Full Text]