<i>msls</i> act early in the female sex determination process, and all key components of the dosage compensation complex, affect female viability.

(A) msl-31 homozygous mothers mated to males mutant for single numerator gene (sis-a1 or sis-bsc3-1) or Sxl early phase (f9) or late phase defective (M1, f12) allele (test class total n = 1135, 1047, 879, 404, 1129, 696, 915, 924, respectively). sis-bsc3-1 cross was done at 29°C, the non-permissive temperature for this temperature-sensitive allele. Percent viability of females relative to their brothers is shown with percentage standard error. Relevant genotype of fathers shown on x-axis. (B) w, sis-bsc3-1, sis-a1, m/FM7 females were mated to either Ore R, mle1/CyO, msl-1L60/CyO, msl-21/CyO, msl-31/TM3, mof2/Y; 18H1[mof+]/+, roX1ex6/Y or roX2−/Y males (test class total n = 420, 241, 208, 285, 363, 447, 408, 418, respectively). Percent viability of sis-a, b/+ females with the msl mutation relative to their FM7/+ sisters also carrying the msl mutation is shown, with percentage standard error. For mof it is for females that did not receive the 18H1[mof+] transgene. Relevant msl genotype of fathers shown on x axis.