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Could be any number of reasons. I'm not a geneticist, but possibilities include:

1) Environmental triggers play a role in the frequency of mutation, and are present to different degrees in sub-Saharan Africa than elsewhere; this mechanism could even hold for racial sub-Saharans who have lived in other parts of the world for many generations, since exposure to particular environmental factors (e.g. types and/or quantities of food) are in part driven by individual choice, which may in turn be driven by a huge number of genetic factors, some of which ar more prevalent in some racial groups than in other.

2) Other genetic factors which are more prevalent in non-sub-Saharans promote the frequency of the mutation;

3) I don't know anything about the specific gene this researcher has identified, but many genes which are especially prone to mutation (including the Fragile X gene) involve repeated series of nucleotide triplets which can produce a normal outcome with various numbers of triplets, but beyond a certain number are a) more likely to produce some small but measurable variation in the organism, and b) more prone to mutate further by adding even more extra copies of the triplet, thus producing a marked variation in the organism. In the case of Fragile X, for example, the pre-mutation form of the gene involves a greater than normal number of repetitions of the triplet, but still produces a barely perceptible (or often imperceptible) drag on cognitive function; the full mutation form involves even more copies of the triplet and produces significant mental retardation. Below is an abstract of a medical journal article regarding racial group variations in Fragile X genes, which gives a clue as to how certain groups can have greater susceptibility to a particular type of gene mutation than other groups. The gist is that there can be huge number of variations of a "normal" gene, and certain of those variations may be more prevalent in certain racial/ethnic groups.

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10915764&dopt=Abstract
The cryptic CGG repeat responsible for the fragile X syndrome, located in the 5'-UTR of FMR1, is unique compared with the many other triplet repeat-causing [sic -- this should read "caused", not "causing"] diseases, making it ideal for identifying factors involved in repeat expansion that may be common to other triplet repeat diseases. To date, a number of factors have been identified which may influence repeat instability, including the number and position of interspersed AGGs, length of the 3' pure CGG repeat and haplotype background. However, nearly all such data were derived from studies of Caucasians. Using a large African-American population, we present the only comprehensive examination of factors associated with CGG repeat instability in a non-Caucasian population. Among Caucasians, susceptible alleles were thought to come from those in the intermediate repeat range (41-60 repeats); however, we find that susceptible alleles may come from a larger repeat pool (35-60 repeats) and are better defined by their pure CGG repeat and/or -presence of only one AGG interruption. These results demonstrate the existence of different susceptible alleles among world populations and may account for the similar prevalence of the fragile X syndrome in African-Americans compared with Caucasians despite the lower frequency of inter-mediate sized alleles in the African-American population. Finally, we show that repeat structures among unaffected African-Americans with the most frequent fragile X haplotype background are either pure or contain a single distal interruption. We propose that the lack of a proximal most interruption is a novel factor involved in CGG repeat instability.