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#SOS response

3 public questions tagged with this topic.

Repair Pathway

RecA activates SOS response by inducing cleavage of

RecA forms helical nucleoprotein filament on single-stranded DNA generated at lesion-stalled forks, with ATP stabilizing active extended conformation termed RecA*. Activated filament functions as coprotease enhancing intrinsic autoproteolytic activity of LexA, UmuD, and phage lambda repressor. LexA self-cleavage occurs between alanine 84 and glycine 85 within flexible linker connecting N-terminal DNA-binding domain and C-terminal dimerization domain. Cleavage splits repressor, rendering fragments unable to dimerize and bind SOS box. Consequently operons derepress without RecA directly cutting LexA. Signal transduction links recombinational sensor to transcriptional response essential for stress adaptation.

Ref: PNAS 2021 Cryo-EM RecA-LexA filament structure autocleavage; Alberts Ch.5 RecA coprotease mechanism SOS activation

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Repair Pathway

SOS response is regulated by

SOS response encompasses global induction of more than forty DNA repair and tolerance genes triggered by extensive single-stranded DNA at stalled replication forks. Central negative regulator is LexA repressor, homodimer binding SOS boxes with consensus CTGTN8ACAG in promoter regions, repressing transcription including own lexA gene and recA, uvr, umuDC operons. Under steady growth, LexA maintains low expression. After DNA damage, activated RecA nucleofilament stimulates LexA autocleavage at Ala84-Gly85, causing dissociation from operators and derepression. Temporal induction occurs as LexA affinity varies across promoters, coordinating error-free and error-prone repair sequentially.

Ref: Alberts Molecular Biology of Cell, 7th ed., Chapter 5: SOS regulon LexA repressor control; Scielo 2020 SOS regulation E coli

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Replication in Prokaryotes

DNA polymerase V is part of

Severe DNA damage causes accumulation of single-stranded DNA activating RecA to stimulate autocleavage of LexA repressor derepressing over 40 SOS genes regulon. Among strongly induced are umuD and umuC genes encoding Pol V, Y-family error-prone polymerase capable of copying past pyrimidine dimers that block Pol III. Pol V requires RecA nucleoprotein filament for activation as mutasome complex. Its expression relatively late in SOS response provides last-resort translesion synthesis when excision repair incomplete enabling survival despite persisting lesions but dramatically increasing mutation rate.

Ref: Lewin Genes XII, Chapter 16: SOS response induction of Pol V UmuC-D for translesion synthesis

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