Knowledge of the structure and function of a complex gene regulating sexual development in the mushroom, Schizophyllum commune, has come from the analysis of various mutations in a chromosomal region known as the BJ3 incompatibility gene. This gene is one of two linked genes, Ba and Bfl, that together comprise the B factor which regulates a developmental sequence known as the B-sequence. The B-sequence is normally "turned off" (Fig. 1 a-e), and each factor controls a part of the series (2). The Asequence comprises nuclear pairing (b), conjugate division (c), and formation of hook cell (c and d), and converges with the B-sequence in fusion of hook cell (e). The B-sequence consists of nuclear migration (a) and fusion of hook cells (e). Sexual development thus requires the operation of both Aand B-sequences, or A-on-B-on. The converse, no sexual expression in unmated haploid strains or in matings homozygous for A and B, is A-off-B-off.Profound biochemical alterations underlie the operation of the sequences and suggest shifts in the spectrum of genes expressed in the morphogenetic progression (3).The present report is concerned with regulatory activity of the B factor and the status of the B-sequence, B-off or B-on; consequently, the status of the A-sequence can be essentially ignored. The terms "off" and "on" as used here signify only the inactivity or operation of the developmental sequence; they are not meant to imply anything about the mode of action of the incompatibility factors.The two genes of the B factor, Ba and Bof, each with nine 1427 known alleles (4), appear to be functionally identical and to act independently. Thus, the matings B al-f#l x B al-#2, B al-#l x B a2-01, and B a3-#4 x B a5-36 lead to a common result: to "turn on" the B-sequence and the characteristic B-on morphology. Matings homozygous for a single B factor, e.g., B a3-f32 x B a3S-#2 fail to turn on the B-sequence, and the phenotype remains B-off.The manner in which the genes of the B factor operate to control the B-sequence of sexual morphogenesis is unknown, but a study of the mutative capabilities provides some clues. All of many mutant alleles recovered in a system designed to select for a change from B-off to B-on were constitutive for the B-sequence (5, 6). The selective system would also have revealed mutations to new wild-type alleles capable of interacting with the progenitor allele to turn on the B-sequence, but no such mutation was found. Each of the mutants in isolation has a continuously operating B-sequence, e.g., the mutation of wild allele B,#2----+ B#2(1) (the number in parentheses representing a type of mutation) renders the B-sequence always on and makes the mutant allele interactive with all wild Bf3 alleles, the progenitor Bg2 included. The B-always-on phenotype is characterized by stunted growth, irregular branching, disrupted septa, and continuous nuclear migration; when the A-sequence is also operative, B-always-on elicits fusion of hook cells (7).Several secondary mutations induced in mutant B-on alleles ...