How we are reshuffling our genome

is an exciting question that will have a large disease relevance. I think this is not so much about cytogenetic abnormalities but the general understanding which genetic modules are recombining, e.g. are compatible in terms of function, and which need to be tight together.
So far, we had only a very crude picture based on microsatellite recombination maps. This changed by the last week with the publication of a SNP based recombination map.

High-Resolution Mapping of Crossovers Reveals Extensive Variation in Fine-Scale Recombination Patterns Among Humans … This analysis revealed that overall recombination hotspot usage is similar in males and females, with individual hotspots often active in both sexes. Across the genome, roughly 60% of crossovers occurred in hotspots inferred from LD studies.

I would recommend to start with the 28 page supplement instead of the 3 page published paper (where mainly Fig.2 -the distribution of recombination from the transcription start sites is being impressive).
Anyway I was particular interested in the identification hotspot motifs as published already in 2005. There seems to be also an update from the earlier description

We found interesting differences in the frequency of certain sequence features between hotspots and coldspots (4). For example, the long terminal repeats of two retrovirus-like retrotransposons, THE1A [frequency in hotspot/frequency in coldspot (RR) = 2.3] and THE1B (RR = 1.7), are strongly overrepresented in hotspots, as are CT-rich repeats (RR = 1.4) and GA-rich repeats (RR = 1.4).

as according to unpublished observations this motif has been extended to a degenerate 13mer. I could not resist, downloaded the Hutterite recombination positions, constructing minimum tiling intervals, downloaded the Fasta sequence and was stopped only by the size limits of the MEME and GIBBS SAMPLER motif search. The story is still not clear how we are reshuffling our genome.
A companion paper in Science at least had another nice idea – to look for a genomic control of genome-wide recombination. Whatever that means – are these the RNF212+ guys driving our evolution? Certainly a dangerous idea …