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Literature summary for 3.4.21.88 extracted from

  • Fornelos, N.; Butala, M.; Hodnik, V.; Anderluh, G.; Bamford, J.K.; Salas, M.
    Bacteriophage GIL01 gp7 interacts with host LexA repressor to enhance DNA binding and inhibit RecA-mediated auto-cleavage (2015), Nucleic Acids Res., 43, 7315-7329 .
    View publication on PubMedView publication on EuropePMC
Search for more literature for 3.4.21.88

Activating Compound

Activating Compound Comment Organism Structure
GIL01 phage gp7 protein LexA is unable to efficiently repress GIL01 transcription unless the small phage-encoded protein gp7 is also present. Phage protein gp7 forms a stable complex with LexA that enhances LexA binding to phage and cellular SOS sites and interferes with RecA-mediated auto-cleavage of LexA, the key step in the initiation of the SOS response. Gp7 does not bind DNA, alone or when complexed with LexA. Gp7 interacts with LexA at dinBox1 and dinBox1b and Gp7 induces a LexA conformation that favors DNA binding but disfavors LexA auto-cleavage, thereby altering the dynamics of the cellular SOS response. Gp7 increases the apparent binding capacity of LexA for din-Box1 and dinBox1b. Gp7 represses promoter P1 and prevents its SOS induction in vivo. gp7 repression of P1 is LexA-dependent Bacillus thuringiensis serovar israelensis
additional information LexA activation by activated RecA-dependent proteolytic self-cleavage Bacillus thuringiensis serovar israelensis

Cloned(Commentary)

Cloned (Comment) Organism
gene lexA, overexpression of His6-tagged enzyme in Escherichia coli strain M15 Bacillus thuringiensis serovar israelensis

Natural Substrates/ Products (Substrates)

Natural Substrates Organism Comment (Nat. Sub.) Natural Products Comment (Nat. Pro.) Rev. Reac.
additional information Bacillus thuringiensis serovar israelensis LexA binds to dinBox1 and to half-site dinBox1b in the SOS boxes in the lysogenic promoter P1 of phage GIL01. The dinBox1 is a 14-bp long sequence in the P1 promoter region that is similar to the consensus LexA binding site in Bacillus subtilis (CGAAC(n)4GTTCG). Transcription from promoter P1 is regulated by host LexA and phage-borne factors ?
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 ?
additional information Bacillus thuringiensis serovar israelensis ATCC 35646 LexA binds to dinBox1 and to half-site dinBox1b in the SOS boxes in the lysogenic promoter P1 of phage GIL01. The dinBox1 is a 14-bp long sequence in the P1 promoter region that is similar to the consensus LexA binding site in Bacillus subtilis (CGAAC(n)4GTTCG). Transcription from promoter P1 is regulated by host LexA and phage-borne factors ?
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 ?

Organism

Organism UniProt Comment Textmining
Bacillus thuringiensis serovar israelensis Q3ET60 G9842
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Bacillus thuringiensis serovar israelensis ATCC 35646 Q3ET60 G9842
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Posttranslational Modification

Posttranslational Modification Comment Organism
proteolytic modification recombinant activated RecA-dependent LexA repressor self-cleavage Bacillus thuringiensis serovar israelensis

Purification (Commentary)

Purification (Comment) Organism
recombinant His6-tagged enzyme from Escherichia coli strain M15 by nickel affinity chromatography and ultrafiltration Bacillus thuringiensis serovar israelensis

Substrates and Products (Substrate)

Substrates Comment Substrates Organism Products Comment (Products) Rev. Reac.
additional information LexA binds to dinBox1 and to half-site dinBox1b in the SOS boxes in the lysogenic promoter P1 of phage GIL01. The dinBox1 is a 14-bp long sequence in the P1 promoter region that is similar to the consensus LexA binding site in Bacillus subtilis (CGAAC(n)4GTTCG). Transcription from promoter P1 is regulated by host LexA and phage-borne factors Bacillus thuringiensis serovar israelensis ?
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 ?
additional information LexA binds to dinBox1 and to half-site dinBox1b in the SOS boxes in the lysogenic promoter P1 of phage GIL01. The dinBox1 is a 14-bp long sequence in the P1 promoter region that is similar to the consensus LexA binding site in Bacillus subtilis (CGAAC(n)4GTTCG). Transcription from promoter P1 is regulated by host LexA and phage-borne factors Bacillus thuringiensis serovar israelensis ATCC 35646 ?
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 ?

Synonyms

Synonyms Comment Organism
LexA
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 Bacillus thuringiensis serovar israelensis

Temperature Optimum [°C]

Temperature Optimum [°C] Temperature Optimum Maximum [°C] Comment Organism
37
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 assay at Bacillus thuringiensis serovar israelensis

pH Optimum

pH Optimum Minimum pH Optimum Maximum Comment Organism
7.4
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 assay at Bacillus thuringiensis serovar israelensis

General Information

General Information Comment Organism
physiological function the SOS response in Eubacteria is a global response to DNA damage and its activation is increasingly associated with the movement of mobile genetic elements. The temperate phage GIL01, a parasite of the bacterium, is induced into lytic growth using the host's SOS response to genomic stress. LexA, the SOS transcription factor, represses bacteriophage transcription by binding to a set of SOS boxes in the lysogenic promoter P1. LexA is unable to efficiently repress GIL01 transcription unless the small phage-encoded protein gp7 is also present. Phage protein gp7 forms a stable complex with LexA that enhances LexA binding to phage and cellular SOS sites and interferes with RecA-mediated auto-cleavage of LexA, the key step in the initiation of the SOS response. Gp7 does not bind DNA, alone or when complexed with LexA. Gp7 interacts with LexA at dinBox1 and dinBox1b and Gp7 induces a LexA conformation that favors DNA binding but disfavors LexA auto-cleavage, thereby altering the dynamics of the cellular SOS response. Gp7 increases the apparent binding capacity of LexA for din-Box1 and dinBox1b Bacillus thuringiensis serovar israelensis