Until recently, there were only two known pathways to process Okazaki fragments.

There are two pathways that have been proposed to process Okazaki fragments.

The method was also used to prove the existence and function of Okazaki fragments.

Prokaryotes have Okazaki fragments that are quite longer than those of eukaryotes.

These primers serve as substrates for the synthesis of Okazaki fragments.

The lengths of Okazaki fragments in prokaryotes and eukaryotes are different as well.

Another study investigated the formation of Okazaki fragments in wild-type bacteria cells.

In contrast, lagging strand synthesis is accomplished in short Okazaki fragments.

This causes the formation of Okazaki fragments.

Okazaki fragments are also produced much quicker in prokaryotes since prokaryotic cells contain less genetic material.

Formation of phosphodiester bonds at gaps between Okazaki fragments (ligase)

Flap endonuclease 1 (FEN1) is responsible for processing Okazaki fragments.

Okazaki fragments that are not ligated could cause double-strand-breaks, which cleaves the DNA.

Based on the dangers associated with a failure in the DNA process, Okazaki fragments maintain our evolutionary development.

This alternative pathway occurs when the Pif1 helicase removes entire Okazaki fragments initiated by fold back flaps.

The complexity of the DNA in eukaryotes calls for a longer production time of the Okazaki fragments.

Processing of Okazaki fragments is therefore very common and crucial for DNA replication and cell proliferation.

This includes preventing and removing the strand displacement of 5' flaps, and creating ligatable nicks at the border of Okazaki fragments.

This process is referred to as 'maturation of Okazaki fragments', and ligase (see below) completes the final step in the maturation process.

This means that the piecewise generation of Okazaki fragments can keep up with the continuous synthesis of DNA on the leading strand.

An enzyme called ligase connects the gap in the backbone by forming a phosphodiester bond between each gap that separates the Okazaki fragments.

The interaction between DnaG and DnaB is necessary to control the longitude of Okazaki fragments on the lagging strand.

Primase adds RNA primers onto the lagging strand, which allows synthesis of Okazaki fragments from 5' to 3'.

Pol α is responsible for the initiation of DNA replication at origins and during lagging-strand synthesis of Okazaki fragments.

DNA polymerase on the lagging strand also has to be continually recycled to construct Okazaki fragments following RNA primers.