Fusing worm chromosomes shrinks the genetic map.

Hillers/Elsevier

When it comes to crossover recombination during meiosis, once is usually enough. Most worm chromosomes form one and only one crossover between homologues during meiosis I, and other eukaryotes spread out their crossovers so that only a few form. Now, Kenneth Hillers and Anne Villeneuve (Stanford University, Stanford, CA) find that the worm's once-only rule applies even to fusion chromosomes that contain nearly half of the genome.

The fusions—between either two or three worm chromosomes—resulted in a shrinkage of the genetic map, so that the giant chromosomes showed an average of one crossover each. This suggests that crossover formation is not sequence specific, and that the mechanism that inhibits formation of more than one crossover can spread over entire enlarged chromosomes.

The spreading capability is tempered in heterozygotes. In these cases, with one giant chromosome lined up with its two unfused partners in a trivalent, about half of the meioses had one crossover per trivalent, and half had two crossovers (one crossover for each of the two original [unfused] chromosomes). Spreading fails completely when the middle of three chromosomes can no longer line up with a triple fusion giant chromosome.

In both double and triple fusion homozygotes, as with wild type, there were very few instances in which no crossovers formed. Hillers suggests that the mechanism that ensures this result—at least one crossover—may lead inevitably to only one crossover. For example, Nancy Kleckner (Harvard University, Cambridge, MA) has proposed that chromatin condensation occurring during pairing of chromosomes may exert tension along the lengths of chromosomes, with this tension promoting crossovers. A single recombination event would then release that tension and greatly reduce the likelihood of further recombination. The current results, say Hillers, are consistent with this idea, because they imply a role for the chromosomal axis in transmitting the crossover signal. ▪

Reference:

Hillers, K.J., and A.M. Villeneuve.
2003
.
Curr. Biol.
13
:
1641
–1647.