<P> DNA molecules in eukaryotes differ from the circular molecules of prokaryotes in that they are larger and usually have multiple origins of replication . This means that each eukaryotic chromosome is composed of many replicating units of DNA with multiple origins of replication . In comparison, the prokaryotic E. coli chromosome has only a single origin of replication . In eukaryotes, these replicating forks, which are numerous all along the DNA, form "bubbles" in the DNA during replication . The replication fork forms at a specific point called autonomously replicating sequences (ARS). Eukaryotes have a clamp loader complex and a six - unit clamp called the proliferating cell nuclear antigen . The efficient movement of the replication fork also relies critically on the rapid placement of sliding clamps at newly primed sites on the lagging DNA strand by ATP - dependent clamp loader complexes . This means that the piecewise generation of Okazaki fragments can keep up with the continuous synthesis of DNA on the leading strand . These clamp loader complexes are characteristic of all eukaryotes and separate some of the minor differences in the synthesis of Okazaki fragments in prokaryotes and eukaryotes . The lengths of Okazaki fragments in prokaryotes and eukaryotes are different as well . Prokaryotes have Okazaki fragments that are quite longer than those of eukaryotes . Eukaryotes typically have Okazaki fragments that are 100 to 200 nucleotides long, whereas prokaryotic E. coli can be 2,000 nucleotides long . The reason for this discrepancy is unknown . </P> <P> Although cells undergo multiple steps in order to ensure there are no mutations in the genetic sequence, sometimes specific deletions and other genetic changes during Okazaki fragment maturation go unnoticed . Because Okazaki fragments are the set of nucleotides for the lagging strand, any alteration including deletions, insertions, or duplications from the original strand can cause a mutation if it is not detected and fixed . Other causes of mutations include problems with the proteins that aid in DNA replication . For example, a mutation related to primase affects RNA primer removal and can make the DNA strand more fragile and susceptible to breaks . Another mutation concerns polymerase α, which impairs the editing of the Okazaki fragment sequence and incorporation of the protein into the genetic material . Both alterations can lead to chromosomal aberrations, unintentional genetic rearrangement, and a variety of cancers later in life . </P> <P> To test the effects of the protein mutations on living organisms, researchers genetically altered lab mice to be homozygous for another mutation in protein related to DNA replication, flap endonuclease 1, or FEN1 . The results varied based on the specific gene alterations . Homozygous knockout mutant mice experienced a "failure of cell proliferation" and "early embryonic lethality" (27). Mice with mutation F343A and F344A (also known as FFAA) died directly after birth due to complications including pancytopenia and pulmonary hypoplasia . This is because the FFAA mutation keeps FEN1 from interacting with PCNA (proliferating cell nuclear antigen), consequently not allowing it to complete its purpose during Okazaki fragment maturation . Under careful observation, cells homozygous for FFAA FEN1 mutations seem to display only partial defects in maturation, meaning mice heterozygous for the mutation would be able to survive into adulthood, despite sustaining multiple small nicks in their genomes . Inevitably however, these nicks prevent future DNA replication because the break causes the replication fork to collapse and causes double strand breaks in the actual DNA sequence . In time, these nicks also cause full chromosome breaks, which could lead to severe mutations and cancers . Other mutations have been implemented with altered versions of Polymerase α, leading to similar results . </P>

An okazaki fragment has which of the following