Revisiting the Role of the Male-Specific Lethal Complex in the Sex Determination Decision of Drosophila

(2010) observed strong female lethality but Erickson, using common alleles, did not. Since sex determination is dose-sensitive, Erickson also tested the heterozygous condition over balancers, and found no differences in female-lethal synergism between homozygous and heterozygous msl mothers. 3.Erickson demonstrated that the original msl- 31 background has an additional mutation that strongly synergizes with mutations in the sex determination pathway. In an XSE doublemutant cross, it alone lowers female viability to 2.5%, more than ninefold lower than nonbalancer sisters (unpublished observation). [...]msl homozygous to heterozygous comparisons for dose-sensitive interactions with sex determination genes appear "negative," as the effects are masked by balancer lethality. Erickson questioned, "The model postulates that the MSL complex normally elevates expression of the XSEs twofold, effectively providing females with a 4X and males a 2X concentration of XSE proteins... how can it be that msl mutant females activate SxlPe and wild-type males do not, when both should have equivalent 2X levels of XSE proteins?" To answer: (1) not all X chromosome genes are dosage compensated, including some of the primary sex determination genes (e.g., runt; Gergen 1987; Smith et al 2001); (2) males have a Y chromosome that is a sink for chromatin proteins, particularly heterochromatin protein 1a (HP1), which is required for robust female SxlPe expression (Li etai 2011), so its presence will affect the ease by which males can activate the promoter; and (3) having two X chromosomes gives females the option of pairing them, which can affect gene expression.