Tau protects beta in the leading-strand polymerase complex at the replication fork.
Replication forks formed in the absence of the tau subunit of the DNA polymerase III holoenzyme produce shorter leading and lagging strands than when tau is present. We show that one reason for this is that in the absence of tau, but in the presence of the gamma-complex, leading-strand synthesis is no longer highly processive. In the absence of tau, the size of the leading strand becomes proportional to the concentration of beta and inversely proportional to the concentration of the gamma-complex. In addition, the beta in the leading-strand complex is no longer resistant to challenge by either anti-beta antibodies or poly(dA):oligo(dT). Thus, tau is required to cement a processive leading-strand complex, presumably by preventing removal of beta catalyzed by the gamma-complex.
Kim
S
S
Graduate Program in Molecular Biology, Cornell University Graduate School of Medical Sciences, New York, New York 10021, USA.
Dallmann
H G
HG
McHenry
C S
CS
Marians
K J
KJ
D004258:DNA Polymerase III / Q000378:metabolism*; D004261:DNA Replication; D004269:DNA, Bacterial / Q000096:biosynthesis; D004270:DNA, Circular / Q000096:biosynthesis; D004926:Escherichia coli / Q000235:genetics / Q000378:metabolism*; D007700:Kinetics; D018741:Replication Origin; D013698:Templates, Genetic; D014157:Transcription Factors / Q000378:metabolism*
D004269:DNA, Bacterial; D004270:DNA, Circular; D014157:Transcription Factors; C041273:transcription factor tau; D004258:DNA Polymerase III