[The mechanism of the interchromsomal effect on crossing over in Drosophila melanogaster: delayed crossing over].

Interchromosomal effect on crossing-over (IEC) in autosome 2 has been studied in 2/F(2L); F(2R) females heterozygous for free arms (acrocentrics) and in Is(Y;2)419/+ females with an insertion of Y-material into the region 34A. IEC was induced by In(1)dl-49 + BM1 inversion. Manifestations of IEC included increased recombinational length of chromosome 2 and decreased interference. IEC was not observed in Df(2L)TW161/+ females with 38A-40 deletion. The patterns of IEC in three types of gametes of the 2/F(2L); F(2R) female depended on the pairing relations of the affected chromosome (chromosome-responder). In the case of normal pairing between the metacentric autosome 2 (the metacentric) and the F(2R) acrocentric, the increment in 2R length was minimal (20%), and the increment in the proportion of multiple-exchange (high-rank) tetrads (E2 + E3), maximal (8 to 10%). In the case of disturbed pairing 2-F(2R) nondisjunction, 2R length was increased by 77%, paralleled by a minimal increase in the proportion of high-rank tetrads (4%). Similarly, in females with the insertion, a pronounced increase in 2L length (74%) was associated with a moderate level of high-rank tetrads. When pairing in the chromosome-responder was normal, the increment in crossing-over was maximal in the pericentromeric region. In the case of disturbed pairing, this maximum either shifted toward the middle of the arm 2-F(2R) nondisjunction, or occupied a distal position (in females with the insertion). It is concluded that IEC pattern depends on the order of pairing in the chromosome-responder. The mechanism of IEC appears to be related to pairing "defects" within the responder. It is tempting to speculate that the onset of crossing-over is a whole-cell event, which is regulated by the overall level of chromosome pairing within the meiotic cell. Chromosomal aberrations increase the time required for attaining this level, and the start of crossing-over is delayed. As a result, (1) exchanges are observed in the regions of late synapsis, which are usually not involved in crossing-over; (2) overabundance of recombination enzymes, caused by delayed start of crossing-over, creates the conditions for decreased interference in paired regions.