Lytic gene expression in the temperate bacteriophage GIL01 is activated by a phage-encoded LexA homologue

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Lytic gene expression in the temperate bacteriophage GIL01 is activated by a phage-encoded LexA homologue. / Fornelos, Nadine; Browning, Douglas F; Pavlin, Anja; Podlesek, Zdravko; Hodnik, Vesna; Salas, Margarita; Butala, Matej.

In: Nucleic Acids Research, Vol. 46, No. 18, 12.10.2018, p. 9432–9443.

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Fornelos, Nadine ; Browning, Douglas F ; Pavlin, Anja ; Podlesek, Zdravko ; Hodnik, Vesna ; Salas, Margarita ; Butala, Matej. / Lytic gene expression in the temperate bacteriophage GIL01 is activated by a phage-encoded LexA homologue. In: Nucleic Acids Research. 2018 ; Vol. 46, No. 18. pp. 9432–9443.

Bibtex

@article{76f648e1f62f4401a9cab5e0c4d9e165,
title = "Lytic gene expression in the temperate bacteriophage GIL01 is activated by a phage-encoded LexA homologue",
abstract = "The GIL01 bacteriophage is a temperate phage that infects the insect pathogen Bacillus thuringiensis. During the lytic cycle, phage gene transcription is initiated from three promoters: P1 and P2, which control the expression of the early phage genes involved in genome replication and P3, which controls the expression of the late genes responsible for virion maturation and host lysis. Unlike most temperate phages, GIL01 lysogeny is not maintained by a dedicated phage repressor but rather by the host's regulator of the SOS response, LexA. Previously we showed that the lytic cycle was induced by DNA damage and that LexA, in conjunction with phage-encoded protein gp7, repressed P1. Here we examine the lytic/lysogenic switch in more detail and show that P3 is also repressed by a LexA-gp7 complex, binding to tandem LexA boxes within the promoter. We also demonstrate that expression from P3 is considerably delayed after DNA damage, requiring the phage-encoded DNA binding protein, gp6. Surprisingly, gp6 is homologous to LexA itself and, thus, is a rare example of a LexA homologue directly activating transcription. We propose that the interplay between these two LexA family members, with opposing functions, ensures the timely expression of GIL01 phage late genes.",
author = "Nadine Fornelos and Browning, {Douglas F} and Anja Pavlin and Zdravko Podlesek and Vesna Hodnik and Margarita Salas and Matej Butala",
year = "2018",
month = oct,
day = "12",
doi = "10.1093/nar/gky646",
language = "English",
volume = "46",
pages = "9432–9443",
journal = "Nucleic Acids Research",
issn = "0305-1048",
publisher = "Oxford University Press",
number = "18",

}

RIS

TY - JOUR

T1 - Lytic gene expression in the temperate bacteriophage GIL01 is activated by a phage-encoded LexA homologue

AU - Fornelos, Nadine

AU - Browning, Douglas F

AU - Pavlin, Anja

AU - Podlesek, Zdravko

AU - Hodnik, Vesna

AU - Salas, Margarita

AU - Butala, Matej

PY - 2018/10/12

Y1 - 2018/10/12

N2 - The GIL01 bacteriophage is a temperate phage that infects the insect pathogen Bacillus thuringiensis. During the lytic cycle, phage gene transcription is initiated from three promoters: P1 and P2, which control the expression of the early phage genes involved in genome replication and P3, which controls the expression of the late genes responsible for virion maturation and host lysis. Unlike most temperate phages, GIL01 lysogeny is not maintained by a dedicated phage repressor but rather by the host's regulator of the SOS response, LexA. Previously we showed that the lytic cycle was induced by DNA damage and that LexA, in conjunction with phage-encoded protein gp7, repressed P1. Here we examine the lytic/lysogenic switch in more detail and show that P3 is also repressed by a LexA-gp7 complex, binding to tandem LexA boxes within the promoter. We also demonstrate that expression from P3 is considerably delayed after DNA damage, requiring the phage-encoded DNA binding protein, gp6. Surprisingly, gp6 is homologous to LexA itself and, thus, is a rare example of a LexA homologue directly activating transcription. We propose that the interplay between these two LexA family members, with opposing functions, ensures the timely expression of GIL01 phage late genes.

AB - The GIL01 bacteriophage is a temperate phage that infects the insect pathogen Bacillus thuringiensis. During the lytic cycle, phage gene transcription is initiated from three promoters: P1 and P2, which control the expression of the early phage genes involved in genome replication and P3, which controls the expression of the late genes responsible for virion maturation and host lysis. Unlike most temperate phages, GIL01 lysogeny is not maintained by a dedicated phage repressor but rather by the host's regulator of the SOS response, LexA. Previously we showed that the lytic cycle was induced by DNA damage and that LexA, in conjunction with phage-encoded protein gp7, repressed P1. Here we examine the lytic/lysogenic switch in more detail and show that P3 is also repressed by a LexA-gp7 complex, binding to tandem LexA boxes within the promoter. We also demonstrate that expression from P3 is considerably delayed after DNA damage, requiring the phage-encoded DNA binding protein, gp6. Surprisingly, gp6 is homologous to LexA itself and, thus, is a rare example of a LexA homologue directly activating transcription. We propose that the interplay between these two LexA family members, with opposing functions, ensures the timely expression of GIL01 phage late genes.

U2 - 10.1093/nar/gky646

DO - 10.1093/nar/gky646

M3 - Article

C2 - 30053203

VL - 46

SP - 9432

EP - 9443

JO - Nucleic Acids Research

JF - Nucleic Acids Research

SN - 0305-1048

IS - 18

ER -