Genetic control of recombination in the silkworm. I. Multigenic control of chromosome 2

Summary Response to selection for particular rates of recombination in the silkworm ( Bombyx mori ) is rapid; from a highly heterogeneous foundation stock Hasimoto achieved, in only 10 generations, a 32 per cent difference between lines selected for high and low recombination between the dominant markers Striped and Yellow in chromosome 2. The present study analyses the difference between Hasimoto’s high and low stocks by means of a set of four factorial F 1 crosses, and all but one of the corresponding eight backcrosses. As there is no recombination in females this method can distinguish the effects on recombination of (i) a large inversion in the marked chromosome (chromosome 2), (ii) genes or small inversions in chromosome 2, (iii) genes in the sex chromosome, (iv) genes in the other autosomes, (v) the cytoplasm. There is no large inversion causing reduced recombination in chromosome 2; the cytoplasm has little, if any effect. A recombination gene (or genes, the analysis does not distinguish) is located in chromosome 2, the high allele being recessive (effect of 6 to 11 per cent). At least one other autosome carries a similar gene, with high recessive (effect of around 8 per cent), and there also appears to be an autosome (or several autosomes) with a low recessive effect of 9 per cent, which may or may not be identical with the other autosome. Further autosomes might be revealed by a more sensitive analysis. There may be a small effect ( high recessive) due to the X chromosome. There is no overall dominance in the genes controlling recombination. The genes appear to be either of the rec type discovered in Neurospora , or general modifiers of genomic recombination. Although supergenes in mimetic butterflies at least do not arise by the tightening of linkage between loosely linked or independent loci, modifiers of the type demonstrated in Bombyx may be very effective in tightening still further the linkage within supergenes that come into existence by the alternative “sieve“ mechanism. If most modifiers of recombination are general in their action, rather than specific to one short length of chromosome, then this may in part explain why the genome does not congeal.