Intriguingly, much like it was observed with microsatellite markers, gene flow seemed to spread foremost to the invaded areas, while the native areas appeared less (Elbe) or not at all admixed (Oder).
Also, although we have used genomic information to spread our markers across the genome, more research is needed to determine to what degree the current assay reflects true genome-wide diversity.
To find out what genetic differences underlie natural variation in hermaphrodite mating frequency, we generated a panel of RILs by interbreeding the N2 and HW wild-type isolates and mapped mating frequency to SNP markers spread across the C. elegans genome (see File S2).
There is also no need for the antibiotic resistance genes that have caused such controversy, raising fears that these "marker" genes might spread to animals and to people, rendering antibiotic drugs unworkable.
Deletions in the ORF14/15 and ORF23/24 variable regions have, however, been used as molecular markers to study patterns of virus spread on intermediate and large spatiotemporal scales [8], [9], [10], [11], [12].
These variations may be used as markers to reconstruct the historical spread of plague.
Genomic deletions of various sizes occur at two loci in the WSSV genome, the ORF14/15 and ORF23/24 variable regions, and these have been used as molecular markers to study patterns of viral spread over space and time.
Even though the AFLP loci we used appear to be largely neutral, these markers are likely to be spread randomly across the nuclear genome, and are therefore more likely to be associated with regions under selection than mtDNA markers.
For example, on chromosome VIII, 18 markers are spread on the top 71 cM while 167 markers are spread on the next 29 cM.
These markers are spread across regions that frequently show LOH in glial tumours.
