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Hence, we speculate that these residues among PriB proteins for binding ssDNA do not need to be precisely conserved.
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Hammarsten and Chu (1998) reported that single-stranded DNA (ssDNA) did not inhibit the binding of dsDNA to Ku but it inhibits the binding of dsDNA to DNA-PK.
The nanotube conjugates with SC and ssDNA did not affect cell proliferation and growth.
In contrast, the mobility of mutant ssDNA did not change because the interaction with PEG-b-ODN was negligible.
However E. coli MutL bound to ssDNA does not seem to diffuse along ssDNA, which is supported by our observations of the identical off-rate between the end-free and the end-blocked ssDNA.
In the case of P. syringae, RecBCD lacking RecD becomes functionally inactive, and hence the inhibitory activity of RecDPs for RecA loading on ssDNA does not arise.
We measured ssDNA at the PDA1 locus, which lies about 30 kb away from the end of ChV-R, because ssDNA does not accumulate at this locus in RAD+ strains but does accumulate if Rad9 function is compromised.
However, the lagging strand ssDNA did not serve as a template to generate Okazaki fragments when Pol α and RPA were present.
In addition, pre-incubation of RPA with ssDNA did not result in a detectable interaction between these two proteins (Supplementary Fig. 3B).
SSB tetramers can bind 35−70 base lengths of ssDNA but do not bind short DNA efficiently.
However, given that our substrate has not been unwound upon binding, and does not contain pre-formed ssDNA overhangs on both strands, we cannot exclude the possibility that other parts of the structure may be involved.
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