11
$\begingroup$

The length of Okazaki fragments in the lagging strand is about 100-200 nucleotides in eukaryotes and about 1000-2000 nucleotides in prokaryotes.

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?

Improve this question
$\endgroup$
9
  • 1
    $\begingroup$ Do you think it has to do something with our dna molecule being linear ? If there are shorter okazaki fragments there will be shorter telomere. There is no need for short okazaki fragments in prokaryotes as their genomes are circular and thus there are no telomeres. $\endgroup$
    – biogirl
    Nov 5, 2013 at 17:29
  • 1
    $\begingroup$ @biogirl I guess it is the length of the telomere portion that is capped-off at every division, that will be reduced with shorter Okazaki fragments. Anyway, improving telomere longevity possibly could be a reason:) $\endgroup$
    – stochastic13
    Nov 5, 2013 at 17:38
  • 3
    $\begingroup$ First off, eukaryotes aren't "more evolved" than prokaryotes, just specialized in different ways. If anything, prokaryotes like E. coli with doubling times of as little as 20 minutes might suggest that they are "more" evolved than slow-growing eukaryotes for the basic aspects of growth, such as DNA replication. So the fact that prokaryotic Okazaki fragments are longer might actually suggest that longer Kkazaki fragments are better for DNA replication efficiency, and that they got shorter in eukaryotes due to some other tradeoff. It's pretty much useless to infer adaptivity in this fashion. $\endgroup$
    – A. Kennard
    Nov 5, 2013 at 20:51
  • 3
    $\begingroup$ @SatwikPasani No worries. Sorry to be pedantic; I've worked exclusively with bacteria so far and I can get overly defensive of the little critters ;) Wish I could help actually answer your (interesting) question! $\endgroup$
    – A. Kennard
    Nov 6, 2013 at 23:51
  • 1
    $\begingroup$ I think you are thinking too much into this. Not everything needs to give an advantage :) There is a famous paper about why one should not assume every part of an organism is meant to give an advantage rspb.royalsocietypublishing.org/content/205/1161/581.abstract I would say the length of fragments is more a result of processivity, binding constant of enzyme doing the priming, enzyme concentration etc rather than it being a result of an adaptation to anything in particular. $\endgroup$
    – von Mises
    Nov 7, 2013 at 21:14

1 Answer 1

Reset to default
5
$\begingroup$

I have found one more possible reason from Bruce Alberts' The Molecular Biology of the Cell: (Ch. 5 page 254)

Nucleosomes are spaced at intervals of about 200 nucleotides pairs along the DNA strand , which may explain why new Okazaki fragments are synthesized on the lagging strand at intervals of 100-200 nucleotides in eukaryotes, instead of 1000-2000 nucleotides as in bacteria.

As already discussed by me and @SatwikPasani in the comments, increasing telomere longevity in eukaryotes by reducing the length of okazaki fragments, and consequently reducing the part of telomere cut-off after every division might be another reason for having shorter fragments in eukaryotes as compared to prokaryotes which do not contain telomeres.

EDIT : Having thought over it again, the relation between Okazaki fragment length and telomeres do not seem logical as only RNA primer length is important when considering telomere length.

Balakrishnan and Bambara (2013) explain the regulation of (and differences between) prokaryotic and eukaryotic Okazaki fragments in detail.

Improve this answer
$\endgroup$
5
  • 1
    $\begingroup$ @satwik I was thinking over this question again and I think what I said about telomere length is wrong. Okazaki fragments don't influence telomere length, it is just the RNA primer of the lagging strand which is not replaced and thus leads to shorter telomeres. So, I don't see any relation between shorter Okazaki fragments and telomeres. What say ? $\endgroup$
    – biogirl
    Jun 16, 2014 at 10:41
  • $\begingroup$ @satwik But it would be interesting to find out whether the RNA Primers used in eukaryotes are shorter than those used in prokaryotes. $\endgroup$
    – biogirl
    Jun 16, 2014 at 10:44
  • $\begingroup$ true. I would certainly be interested in finding a similar trend of lengths for the primers. $\endgroup$
    – stochastic13
    Jun 16, 2014 at 10:57
  • $\begingroup$ @biogirl I was wondering the same thing regarding variation in the length of Okazaki fragments. Your discussion has been helpful. Thanks. As you mentioned, did you find any relation between variation in the length of RNA primer and telomere longevity? $\endgroup$
    – Ramil
    Sep 29, 2016 at 16:42
  • $\begingroup$ An addition: the lagging strand synthesis involves bending of the ssDNA such that it aligns in the direction of the replication fork. The nucleosomes (and the condensed eukaryotic chromatin) can hinder this bending such that only short stretches of bent ssDNA is available for the lagging strand synthesis. $\endgroup$
    – WYSIWYG
    Aug 30, 2018 at 14:34

You must log in to answer this question.

Not the answer you're looking for? Browse other questions tagged .