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At the birth of molecular radiation biology
Author(s) -
Devoret Raymond
Publication year - 2001
Publication title -
environmental and molecular mutagenesis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1
H-Index - 87
eISSN - 1098-2280
pISSN - 0893-6692
DOI - 10.1002/em.1064
Subject(s) - repressor lexa , prophage , sos response , biology , repressor , dna repair , genetics , dna replication , dna , nucleotide excision repair , pyrimidine dimer , dna damage , microbiology and biotechnology , gene , bacteriophage , escherichia coli , transcription factor
Rational thinking builds on feelings, too. This article starts with a tribute to Richard Setlow, an eminent scientist; it retraces as well some studies in molecular genetics that helped to understand basic questions of radiation biology. In the mid‐1950s, the induction of a dormant virus (prophage) by irradiation of its host was an intriguing phenomenon. Soon, it was found that prophage induction results from the inactivation of the prophage repressor. Similarly, a score of induced cellular SOS functions were found to be induced when the LexA repressor is inactivated. Repressor inactivation involves the formation of a newly formed distinctive structure: a RecA‐polymer wrapped around single‐stranded DNA left by the arrest of replication at damaged sites. By touching this RecA nucleofilament, the LexA repressor is inactivated, triggering the sequential expression of SOS functions. The RecA nucleofilament acts as a chaperone, allowing recombinational repair to occur after nucleotide excision repair is over. The UmuD′C complex, synthesized slowly and parsimoniously, peaks at the end of recombinational repair, ready to be positioned at the tip of a RecA nucleofilament, placing the UmuD′C complex right at a lesion. At this location, UmuD′C prevents recombinational repair, and now acts as an error‐prone paucimerase that fills the discontinuity opposite the damaged DNA. Finally, the elimination of lesions from the path of DNA polymerase, allows the resumption of DNA replication, and the SOS repair cycle switches to a normal cell cycle. Environ. Mol. Mutagen. 38:135–143, 2001. © 2001 Wiley‐Liss, Inc.