The salivary gland cells of Sxl^f1/Sxl^fhv1 females show somatic mosaicism; some cells are of "male" type (Sxl is not expressed), while others are of "female" type (Sxl is expressed). The frequency of weak spots in the intercalary heterochromatin regions of the X chromosomes is much lower in the "male" cells compared to in the "female" cells and bands of intercalary heterochromatin in the X chromosome look solid, dense and non-broken in the "male" cells, as occurs in normal males.

A few percent of the Sxl^f1/Sxl^fhv1 female progeny survive to the third larval instar stage.

Females of the genotype Sxl^f1/Sxl^fhv1 fail to activate the Sxl locus in a subset of their cells and thus are mosaic for cells that follow either the male of female pathway for dosage compensation. In XX cells that have adopted the male fate msl-2 interacts in a full male-like pattern. Mosaics lacking mle or msl-3 show partial immunostaining patterns for msl-2. msl-1 and msl-2 precisely colocalise at the msl-3 and mle independent sites. msl-2 localisation is completely abolished in the absence of msl-1.

Heterozygous Sxl^f1/Sxl^fhv1 female larvae are mosaics of male and female cells.

50% females heteroallelic for Sxl^f1 and Sxl^fhv1 survive to the third instar larval stage and are mosaic for Sxl expression.

Viability of Sxl^f1/Sxl^fhv1 females reduced compared to wild type, but some individuals survive into larvae and a few survive to adult hood. The larvae are mosaic for Sxl function: Sxl protein is bound to X chromosomes in approximately half of the cells in the salivary glands, mle protein is bound to X chromosomes in those cells where Sxl is not. Sxl^f1/Sxl^fhv1 females that are also homozygous for mutants at msl-1, msl-2 or msl-3 develop as intersexes of the mosaic type.

A subliminal allele, viable and fertile as homozygous females, but with greatly reduced viability in trans to nulls. Polytene chromosomes of Sxl^fhv1/Sxl^f1 larvae that survive to third instar hyperincorporate uridine, revealing female dosage compensation upsets. Mutation of mle appears to partially masculinize this heteroallelic combination and may slightly increase viability under some conditions. Sxl^fhv1 homozygotes and heterozygotes display an increased requirement for maternal da⁺ activity, suggestive of defects in early Sxl regulation.