Genetic control of damage-inducible restriction alleviation in Escherichia coli K12: an SOS function not repressed by lexA

Abstract

The alleviation of K-specific DNA restriction after treatment of cells by UV or nalidixic acid has been studied in mutants with various alleles of recA and lexA and combinations of these alleles and with recB and recF mutations. The studies show that induction of restriction alleviation by UV or nalidixic acid is abolished in mutants in which the recA protein is defective (recA13, recA56), its protease activity is altered (recA430) or in which it cannot be efficiently activated (recA142). Thermoinduction of restriction alleviation was observed in tif mutant (recA441). In lexA amber mutants restriction alleviation is not constitutive but is still inducible. In a lexA3 mutant restriction alleviation is inducible by nalidixic acid provided that recA protein is overproduced as a result of a recA operator mutation. Induction by UV depends on the recF function and an unidentified function (Y) which is controlled by the lexA protein. The recBC enzyme is necessary for induction by UV or by nalidixic acid. Temperature shift experiments with a thermosensitive recB mutant indicate that the recBC enzyme functions in an early step during UV-induction. It is concluded that the damage-inducible function which alleviates restriction is similar to other damage inducible repair (SOS) functions in the dependence on activated recA protease for induction, but that it differs from these functions by the absence of a direct control through the lexA repressor.

Immigration control of DNA in bacteria: self versus non-self

“…A similar response has been demonstrated for a variety of agents that damage DNA, including mutagens such as the base analogue 2-aminopurine (2-AP), and defects in some genes that affect DNA metabolism, e.g. dam, topA and mutD (dnaQ) (Efimova et al, 1988a, b ;Thoms & Wackernagel, 1984 ;Makovets et al, 1999). DNA damage may generate unmodified target sequences as a consequence of the repair of double-strand breaks by homologous recombination (see Fig.…”

“…Alternatively, RecA protein itself could be necessary for activation of the alleviation pathway. RecA is necessary for the alleviation of restriction in response to UV irradiation (Thoms & Wackernagel, 1984 ;Salaj-SB mic et al, 1997) but it is not necessary for the alleviation of restriction in response to treatment with 2-AP (Makovets et al, 1999).…”

Type I Restriction Systems: Sophisticated Molecular Machines (a Legacy of Bertani and Weigle)

“…A temporary loss of restriction proficiency, referred to as restriction alleviation (RA), also occurs in response to treatments that damage DNA (17,38,50,67,177,178). UV light, nalidixic acid, 2-aminopurine (2-AP), and 5-bromouracil have all been shown to induce RA.…”

RloC: A Translation-Disabling tRNase Implicated in Phage Exclusion During Recovery from DNA Damage

“…After all, bacteria normally respond to DNA insults by enhancing the synthesis of DNA repair and other stress responsive proteins (Fernandez De Henestrosa et al, 2000). This apparent contradiction may be reconciled by considering the phenomenon of DNA restriction alleviation (RA) (Thoms & Wackernagel, 1984). RA is enacted in response to genotoxic stress as a protective measure www.intechopen.com intended to prevent degradation of self DNA.…”

“…RloC combines structural-functional properties of two unrelated proteins (i) the universal DNA-damageresponsive/DNA-repair protein Rad50/SbcC (Williams et al, 2007) and (ii) the translationdisabling, phage-excluding anticodon nuclease (ACNase) PrrC (Blanga-Kanfi et al, 2006). These seemingly conflicting features may be reconciled in a model where RloC is mobilized as an antiviral back-up function during recovery from DNA damage (Davidov & Kaufmann, 2008), when DNA restriction, the cell's primary immune system is temporarily shut-off (Thoms & Wackernagel, 1984). Another intriguing feature of RloC is its ability to excise its substrate's wobble nucleotide (Davidov & Kaufmann, 2008).…”