Previous evidence from Drosophila mutants has shown that the relationship between recombination and the SC is not the same as it is in yeast. For example, the mei-W68 mutant has a normal SC but does not undergo recombination and the
c(3)G
mutant eliminates both the SC and recombination. To investigate whether recombination depends on the SC, Page and Hawley have cloned c(3)G and shown that it encodes an essential component of the SC. As expected, C(3)G localizes between the paired homologues, and this localization is altered in mutants that disrupt the SC, confirming its role as an integral part of the SC.
Using C(3)G as a marker, Page and Hawley looked at the SC in mutants in which meiotic exchange is defective. One class of these mutants has reduced frequency of exchange, and the distribution of crossover sites is biased against distal parts of the chromosomes — a phenomenon known as polar effect. Because C(3)G is mislocalized in these mutants, the authors conclude that incorrect SC assembly might, at least partially, account for the polar effect. But even in normal cells, crossovers are not randomly distributed along the chromosome because of crossover interference — the suppression of crossovers in the immediate neighbourhood of an established crossover point. In yeast, incorrect assembly of the SC and incomplete pairing of the homologues abolishes interference, but in Drosophila, Page and Hawley show that when the SC is absent because C(3)G is mislocalized or non-functional, interference is essentially unaffected.
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