Control of short leftward transcripts from the immunity and ori regions in induced coliphage lambda

Hayes, Sidney; Szybalski, Waclaw

doi:10.1007/bf00269438

Cited by 140 publications

(50 citation statements)

References 25 publications

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“…To identify the RexB protein, we replaced the natural ribosome-binding site of RexB with an efficient synthetic one (SD8) (Gold and Stormo 1990) and eliminated the promoter, PLIT (Hayes and Szybalski 1973;Landsmann et al 1982), which is located in the carboxyl terminus of the RexA-coding sequence. A polymerase chain reaction (PCR)-amplified DNA molecule corresponding to coding nucleotides 1-392 of the rexB gene was synthesized with upstream Eagl, Sail, and SD8 ribosomebinding sites by using an amino-terminal PCR primer 5'-AAA-AACGGCCGTCCGACTAAACTAAACTAAGGAAGGAAA-AAAAAA TGCCGGAACAGAATCATGCCTGG-3' and a carboxy-terminal primer 3'-GTAGCAAAAGTTAAAGGTTA-ATATACGTAACCTTAGGAAAAAA-5'.…”

Section: Bacteria Phages and Plasmidsmentioning

confidence: 99%

The Rex system of bacteriophage lambda: tolerance and altruistic cell death.

Parma¹,

Snyder²,

Sobolevski³

et al. 1992

Genes Dev.

154

118

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The rexA and rexB genes of bacteriophage A. encode a two-component system that aborts lytic growth of bacterial viruses. Rex exclusion is characterized by termination of macromolecular synthesis, loss of active transport, the hydrolysis of ATP, and cell death. By analogy to colicins El and K, these results can be explained by depolarization of the cytoplasmic membrane. We have fractionated cells to determine the intracellular location of the RexB protein and made RexB-alkaline phosphatase fusions to analyze its membrane topology. The RexB protein appears to be a polytopic transmembrane protein. We suggest that RexB proteins form ion channels that, in response to lytic growth of bacteriophages, depolarize the cytoplasmic membrane. The Rex system requires a mechanism to prevent X itself from being excluded during lytic growth. We have determined that overexpression of RexB in A. lysogens prevents the exclusion of both T4 rll mutants and X ren mutants. We suspect that overexpression of RexB is the basis for preventing self-exclusion following the induction of a \ lysogen and that RexB overexpression is accomplished through transcriptional regulation.

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Section: Bacteria Phages and Plasmidsmentioning

confidence: 99%

The Rex system of bacteriophage lambda: tolerance and altruistic cell death.

Parma¹,

Snyder²,

Sobolevski³

et al. 1992

Genes Dev.

154

118

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“…Therefore, we have focused our attention on in vitro synthesis from XpL8 DNA of a discrete 4S RNA designated "oop" (19). This RNA, which is transcribed from a point near the origin of X replication (20,21), provides an attractive system for several reasons. First, the nucleotide sequence of the 4S RNA as well as the sequence of Xpga18 for approximately 35 nucleotides beyond the 3' end of the transcript have been determined (22).…”

Section: Introductionmentioning

confidence: 99%

Transcription in vitro of bacteriophage lambda 4S RNA: studies on termination and rho protein

1977

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“…1). The genes rexA and rexB can be expressed coordinately with the cI repressor gene from promoters p RM and p RE (5,7,8). However, there is a third promoter, p LIT , that overlaps the region encoding the carboxyl terminus of rexA.…”

mentioning

confidence: 99%

“…However, there is a third promoter, p LIT , that overlaps the region encoding the carboxyl terminus of rexA. Transcription from p LIT results in the synthesis of the lit mRNA, which permits the expression of rexB without that of rexA (5,7,9). This shift from coordinate to discoordinate expression of rexB and rexA implies that rexB may have another function independent of that of rexA (3,5).…”

mentioning

confidence: 99%

rexB of bacteriophage λ is an anti-cell death gene

Engelberg‐Kulka

Reches

Narasimhan

et al. 1998

Proc. Natl. Acad. Sci. U.S.A.

107

100

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In Escherichia coli, programmed cell death is mediated through ''addiction modules'' consisting of two genes; the product of one gene is long-lived and toxic, whereas the product of the other is short-lived and antagonizes the toxic effect. Here we show that the product of rexB, one of the few genes expressed in the lysogenic state of bacteriophage , prevents cell death directed by each of two addiction modules, phd-doc of plasmid prophage P1 and the rel mazEF of E. coli, which is induced by the signal molecule guanosine 3,5-bispyrophosphate (ppGpp) and thus by amino acid starvation. RexB inhibits the degradation of the antitoxic labile components Phd and MazE of these systems, which are substrates of ClpP proteases. We present a model for this anti-cell death effect of RexB through its action on the ClpP proteolytic subunit. We also propose that the rex operon has an additional function to the well known phenomenon of exclusion of other phages; it can prevent the death of lysogenized cells under conditions of nutrient starvation. Thus, the rex operon may be considered as the ''survival operon'' of phage .

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Control of short leftward transcripts from the immunity and ori regions in induced coliphage lambda

Cited by 140 publications

References 25 publications

The Rex system of bacteriophage lambda: tolerance and altruistic cell death.

The Rex system of bacteriophage lambda: tolerance and altruistic cell death.

Transcription in vitro of bacteriophage lambda 4S RNA: studies on termination and rho protein

rexB of bacteriophage λ is an anti-cell death gene

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