Mutations in this gene may have adverse consequences for a person's health but, rather like the mutation of the haemoglobin gene that causes sickle-cell anaemia, they can also protect that individual against malaria.Again like the sickle-cell gene, some G6PD mutations have spread in parts of the world in which malaria is endemic.
The same mutations have spread between the different ISX elements because transposable elements with the mutations have been used to directly convert other ISX elements without them.
However, because the mutations found by Ellison and Bachtrog are beneficial, natural selection tend to favor individuals where the mutation has spread over those where it has been reversed.
Haplotype analysis can provide minimum estimates for the time of origin of a founder mutation; more exactly, of the time when the mutation has spread, presumably because of population bottleneck was followed by expansion.
Now, in eLife, Christopher Ellison and Doris Bachtrog both from the University of California, Berkeley report that a beneficial mutation has spread via these two mechanisms to multiple sites on the X chromosome of the fruit fly Drosophila miranda (Ellison and Bachtrog, 2015).
Resistance of Plasmodium falciparum to the antimalarial drug sulfadoxine pyrimethamine is a result of extremely rare mutations that have spread over large geographical areas.
If mutations in the organellar genome for example changed the properties of the OM pores and made it easier for the host to insert carriers and thereby increase the fitness of the consortium, such mutations could have spread.
Had the two arms of the study not been carried out in parallel, future researchers might have travelled up an expensive and time-consuming blind alley.Another question is why such a disastrous mutation should have spread so widely in Africa.
However, it is difficult to explain how the -14010C mutation could have spread from a putative Kenyan/Tanzanian center of origin into the remote areas of southwestern Angola without reaching neighboring regions in Mozambique, where no lactase persistence variants could be found.
Following the reasoning developed in the previous pages, most of these mutations may thus have spread to the whole populations, but the fixation of some may have involved and/or contributed to the isolation of relatively small groups of individuals from their direct ancestors.
We could hypothesize that the mutation was born in the Middle Est 2,400 years and arrived in European regions approximately at the time of Caesar Augustus when Roman Empire had the maximum expansion: thus, this mutation may then have spread throughout the Mediterranean area and perhaps elsewhere in the Roman Empire (Fig. 4).
