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Male  Drosophila  are monosomic for the X chromosome, but survive due to dosage compensation. They use the Male Specific Lethal (MSL) complex composed of noncoding  roX  RNA and histone modifying enzymes to hypertranscribe most genes along the X ∼1.6–1.8 fold relative to each female allele. It is not known how the MSL complex achieves this precise adjustment to a large and diverse set of target genes. We carried out a genetic screen searching for novel factors that regulate dosage compensation in flies. This strategy generated thirty alleles in a previously uncharacterized gene,  over compensating males  ( ocm ) that antagonizes some aspect of MSL activity. The mutations were initially recovered because they derepressed an MSL-dependent eye color reporter. Null  ocm  mutations are lethal to both sexes early in development revealing an essential function. Combinations of hypomorphic  ocm  alleles display a male specific lethality similar to mutations in the classic  msl  genes, but  ocm  males die due to excessive, rather than lack of dosage compensation. Males that die due to very low MSL activity can be partially rescued by  ocm  mutations. Likewise, males that would die from  ocm  mutations can be rescued by reducing the dose of various  msl  and  roX  genes.  ocm  encodes a large nuclear protein that shares a novel cysteine rich motif with known transcription factors.

The Drosophila Over Compensating Males Gene Genetically Inhibits Dosage Compensation in Males