Limits...
A role for accessory genes rI.-1 and rI.1 in the regulation of lysis inhibition by bacteriophage T4.

Golec P, Wiczk A, Majchrzyk A, Łoś JM, Węgrzyn G, Łoś M - Virus Genes (2010)

Bottom Line: The key element of LIN is an interaction between two phage-encoded proteins, the T holin and the RI antiholin.This interaction is stabilized by RIII.In this report, we demonstrate the results of genetic experiments which suggest a synergistic action of two accessory proteins of bacteriophage T4, RI.-1, and RI.1 with RIII in the regulation of LIN.

View Article: PubMed Central - PubMed

Affiliation: Department of Molecular Biology, University of Gdańsk, Kładki 24, Gdańsk, Poland.

ABSTRACT
Lysis inhibition (LIN) is a known feature of the T-even family of bacteriophages. Despite its historical role in the development of modern molecular genetics, many aspects of this phenomenon remain mostly unexplained. The key element of LIN is an interaction between two phage-encoded proteins, the T holin and the RI antiholin. This interaction is stabilized by RIII. In this report, we demonstrate the results of genetic experiments which suggest a synergistic action of two accessory proteins of bacteriophage T4, RI.-1, and RI.1 with RIII in the regulation of LIN.

Show MeSH

Related in: MedlinePlus

Lysis of bacterial cultures by bacteriophage T4rIII. The plasmids present in bacterial cells are indicated on left side of the figure, and the concentration of inducer is indicated on the top. Filled squares show lysis curves of bacterial cells with indicated plasmid. Open circles show lysis curves of a control experiment with pCattTrE18 lacZ. Experiments were performed with all plasmids constructed in this work. Experiments which are not shown in the figure have given results identical with control experiments at all concentrations of the inducer tested. For the construct of each plasmid, see Table 1
© Copyright Policy
Related In: Results  -  Collection


getmorefigures.php?uid=PMC2962797&req=5

Fig3: Lysis of bacterial cultures by bacteriophage T4rIII. The plasmids present in bacterial cells are indicated on left side of the figure, and the concentration of inducer is indicated on the top. Filled squares show lysis curves of bacterial cells with indicated plasmid. Open circles show lysis curves of a control experiment with pCattTrE18 lacZ. Experiments were performed with all plasmids constructed in this work. Experiments which are not shown in the figure have given results identical with control experiments at all concentrations of the inducer tested. For the construct of each plasmid, see Table 1

Mentions: Contrary to T4rI, T4D lysis profile was sensitive to overexpression of several genes, and in most of cases the lysis profile was also dependent on the dose of the inducer (Fig. 2). The most pronounced elongation of the lysis profile was obtained by overproduction of RIII (Fig. 2, 10–12), especially together with RI.-1 (Fig. 2, 19–21) or RI.1 (Fig. 2, 16–18). When rIII was present on the plasmid together with rI.-1 or rI.1, even a very low level expression, resulting from a leakiness of the promoter, was sufficient to prolong the lysis profile considerably (Fig. 2, 16, 19). When the efficient overexpression system was used, rIII alone caused slowing down of bacterial growth. This effect was not observed when rIII was co-expressed with rI.-1 or rI.1. Efficient overexpression of rIII, rIII together with rI.1, and rIII together with rI.-1 caused a loss of the rapid lysis phenotype, when T4rIII phage was used for infection (Fig. 3, 4–6, 10–12, 13–15). In the same experimental system, an effective prolongation of LIN was observed after infection with T4D (Fig. 2, 10–12, 16–18, 19–21). Results of this set of experiments showed a synergistic effect of rI.1 and rI.-1 in prolongation of LIN when these genes were co-expressed with rIII. Low expression level of rIII alone gave no effect on LIN caused by T4D or T4rIII infection.Fig. 2


A role for accessory genes rI.-1 and rI.1 in the regulation of lysis inhibition by bacteriophage T4.

Golec P, Wiczk A, Majchrzyk A, Łoś JM, Węgrzyn G, Łoś M - Virus Genes (2010)

Lysis of bacterial cultures by bacteriophage T4rIII. The plasmids present in bacterial cells are indicated on left side of the figure, and the concentration of inducer is indicated on the top. Filled squares show lysis curves of bacterial cells with indicated plasmid. Open circles show lysis curves of a control experiment with pCattTrE18 lacZ. Experiments were performed with all plasmids constructed in this work. Experiments which are not shown in the figure have given results identical with control experiments at all concentrations of the inducer tested. For the construct of each plasmid, see Table 1
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC2962797&req=5

Fig3: Lysis of bacterial cultures by bacteriophage T4rIII. The plasmids present in bacterial cells are indicated on left side of the figure, and the concentration of inducer is indicated on the top. Filled squares show lysis curves of bacterial cells with indicated plasmid. Open circles show lysis curves of a control experiment with pCattTrE18 lacZ. Experiments were performed with all plasmids constructed in this work. Experiments which are not shown in the figure have given results identical with control experiments at all concentrations of the inducer tested. For the construct of each plasmid, see Table 1
Mentions: Contrary to T4rI, T4D lysis profile was sensitive to overexpression of several genes, and in most of cases the lysis profile was also dependent on the dose of the inducer (Fig. 2). The most pronounced elongation of the lysis profile was obtained by overproduction of RIII (Fig. 2, 10–12), especially together with RI.-1 (Fig. 2, 19–21) or RI.1 (Fig. 2, 16–18). When rIII was present on the plasmid together with rI.-1 or rI.1, even a very low level expression, resulting from a leakiness of the promoter, was sufficient to prolong the lysis profile considerably (Fig. 2, 16, 19). When the efficient overexpression system was used, rIII alone caused slowing down of bacterial growth. This effect was not observed when rIII was co-expressed with rI.-1 or rI.1. Efficient overexpression of rIII, rIII together with rI.1, and rIII together with rI.-1 caused a loss of the rapid lysis phenotype, when T4rIII phage was used for infection (Fig. 3, 4–6, 10–12, 13–15). In the same experimental system, an effective prolongation of LIN was observed after infection with T4D (Fig. 2, 10–12, 16–18, 19–21). Results of this set of experiments showed a synergistic effect of rI.1 and rI.-1 in prolongation of LIN when these genes were co-expressed with rIII. Low expression level of rIII alone gave no effect on LIN caused by T4D or T4rIII infection.Fig. 2

Bottom Line: The key element of LIN is an interaction between two phage-encoded proteins, the T holin and the RI antiholin.This interaction is stabilized by RIII.In this report, we demonstrate the results of genetic experiments which suggest a synergistic action of two accessory proteins of bacteriophage T4, RI.-1, and RI.1 with RIII in the regulation of LIN.

View Article: PubMed Central - PubMed

Affiliation: Department of Molecular Biology, University of Gdańsk, Kładki 24, Gdańsk, Poland.

ABSTRACT
Lysis inhibition (LIN) is a known feature of the T-even family of bacteriophages. Despite its historical role in the development of modern molecular genetics, many aspects of this phenomenon remain mostly unexplained. The key element of LIN is an interaction between two phage-encoded proteins, the T holin and the RI antiholin. This interaction is stabilized by RIII. In this report, we demonstrate the results of genetic experiments which suggest a synergistic action of two accessory proteins of bacteriophage T4, RI.-1, and RI.1 with RIII in the regulation of LIN.

Show MeSH
Related in: MedlinePlus