Abstract:
:The Escherichia coli dnaN159 allele encodes a mutant form of the beta-sliding clamp (beta159) that is impaired for interaction with the replicative DNA polymerase (Pol), Pol III. In addition, strains bearing the dnaN159 allele require functional Pol I for viability. We have utilized a combination of genetic and biochemical approaches to characterize the role(s) played by Pol I in the dnaN159 strain. Our findings indicate that elevated levels of Pol I partially suppress the temperature-sensitive growth phenotype of the dnaN159 strain. In addition, we demonstrate that the beta clamp stimulates the processivity of Pol I in vitro and that beta159 is impaired for this activity. The reduced ability of beta159 to stimulate Pol I in vitro correlates with our finding that single-stranded DNA (ssDNA) gap repair is impaired in the dnaN159 strain. Taken together, these results suggest that (i) the beta clamp-Pol I interaction may be important for proper Pol I function in vivo and (ii) in the absence of Pol I, ssDNA gaps may persist in the dnaN159 strain, leading to lethality of the dnaN159 DeltapolA strain.
journal_name
J Bacterioljournal_title
Journal of bacteriologyauthors
Maul RW,Sanders LH,Lim JB,Benitez R,Sutton MDdoi
10.1128/JB.00476-07subject
Has Abstractpub_date
2007-07-01 00:00:00pages
4688-95issue
13eissn
0021-9193issn
1098-5530pii
JB.00476-07journal_volume
189pub_type
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journal_title:Journal of bacteriology
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journal_title:Journal of bacteriology
pub_type: 杂志文章
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journal_title:Journal of bacteriology
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journal_title:Journal of bacteriology
pub_type: 杂志文章
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journal_title:Journal of bacteriology
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journal_title:Journal of bacteriology
pub_type: 杂志文章
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更新日期:1977-08-01 00:00:00
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journal_title:Journal of bacteriology
pub_type: 杂志文章
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更新日期:1974-05-01 00:00:00
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pub_type: 杂志文章
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