DNA replication is a primary mechanism for maintaining genome integrity, but it 
serves this purpose best by cooperating with other proteins involved in DNA 
repair and recombination. Unlike leading strand synthesis, lagging strand 
synthesis has a greater risk of faulty replication for several reasons: First, a 
significant part of DNA is synthesized by polymerase alpha, which lacks a 
proofreading function. Second, a great number of Okazaki fragments are 
synthesized, processed and ligated per cell division. Third, the principal 
mechanism of Okazaki fragment processing is via generation of flaps, which have 
the potential to form a variety of structures in their sequence context. 
Finally, many proteins for the lagging strand interact with factors involved in 
repair and recombination. Thus, lagging strand DNA synthesis could be the best 
example of a converging place of both replication and repair proteins. To 
achieve the risky task with extraordinary fidelity, Okazaki fragment processing 
may depend on multiple layers of redundant, but connected pathways. An essential 
Dna2 endonuclease/helicase plays a pivotal role in processing common structural 
intermediates that occur during diverse DNA metabolisms (e.g. lagging strand 
synthesis and telomere maintenance). Many roles of Dna2 suggest that the 
preemptive removal of long or structured flaps ultimately contributes to genome 
maintenance in eukaryotes. In this review, we describe the function of Dna2 in 
Okazaki fragment processing, and discuss its role in the maintenance of genome 
integrity with an emphasis on its functional interactions with other factors 
required for genome maintenance.