What (molecular mechanism, enzyme type ) determines the length of these Okazaki fragments?
Moreover, which, longer or shorter, fragments would be more advantageous (energetically and considering accuracy)?
Longer fragments means less use of DNA ligase, DNA polymerase-I (prokaryotes) and other enzymes required to convert the okazaki fragments with dispersed RNA primers into a normal strand, and hence lesser scope of mistakes during replication in the lagging strand. Shorter Okazaki fragments improve telomere longevity, by reducing the capped-off portion after every division. Which of these views is correct?