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DOI: http://dx.doi.org/10.7554/eLife.02630.022 Large decreases in recombination could be explained if some DSBs are infrequently repaired as crossovers in hybrids, or if the crossovers they produce generate inviable chromosomes, for instance due to chromosomal rearrangements.

By removing a single gene from a mouse's chromosomes, for instance, researchers can pinpoint the gene's function by studying mice who survive without it.

In these branches we observe teleost genes located on the same chromosomes (for instance zebrafish GRIN2A, -2B and - 2C orthologs, all on chromosome 3), likely due to the chromosomal rearrangements.

Certain chromosomes, for instance, appear to have changed little since the divergence of these teleost species (e.g., Danio chromosomes 6 and 23 in Astyanax linkage groups 13 and 15, respectively).

This chromatin model could explain how centromeres from multiple nonhomologous chromosomes, for instance, could cluster kinetochores and enable segregation by a smaller number of spindle microtubules, or how closely positioned adjacent genes could be independently regulated.

The FSCN gene family has several teleost sequences located on the same chromosomes, for instance on zebrafish chromosome 3, medaka chromosome 8 and stickleback linkage group XI, and the FNG family has teleost duplicates in the LFNG cluster.

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Trying to get all mapped reads for a chromosome, for instance, could yield millions of reads, which is too much data to provide to a Web visualization.

However, there could be some degree of selection for keeping co-regulated genes in clusters on a chromosome, for instance, to make them available to transcription more efficient as a group.

Chromosome 4, for instance, has only 2.02% of sequences showing copy number variable, while chromosome 18 has > 18.01% of sequences with copy number variation.

Human chromosome 1, for instance, contains more than 300,000 oligonucleotides covered by the 15-mer claim on BRCA1.

The selective advantage of multiple origins (if any) is not clear: the fact that the origins are unevenly distributed on the chromosome is, for instance, not in agreement with models in which shortening of the replication time would be the main selective force.

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