Sibling control embryos, that are wild type with respect to rox1 and rox2 and are distinguished from the mutant embryos by the ftz-lacZ staining show normal MSL staining. The deletions in the 10B,C region that do not remove the rox2 gene do not show any abnormal MSL distribution when combined with the rox1 mutation. These data thus show that only simultaneous mutations in both rox1 and rox2 abolish MSL association with the X chromosome. Thus it has been established that the rox1 and rox2 RNAs function as integral components in dosage compensation. The findings that the rox1 and rox2 genes have an essential but redundant function in dosage compensation and that these RNAs colocalize with the MSL proteins suggest that they are components of an RNA-protein complex that brings about dosage compensation.
Several results suggest that the rox RNAs are redundant in their function.
The finding that embryos exhibit a normal MSL binding pattern with either one or the other of the rox genes mutated shows that neither of these RNAs alone is required for dosage compensation. A comparison of the two sequences reveals a region of homology within a 30 bp stretch. Screening the GenBank sequence database with these two 30 nt sequences did not detect other sequences with significant homology. These results are not contradictory, but rather indicate that the rox RNAs are important for the association of all the MSL proteins with the X chromosome, perhaps by being required to form a stable compensasome, and also potentially required for the subsequent RNA dependent stable association of MLE with the X chromosome. There are several ways that the rox RNAs could potentially have direct roles in dosage compensation.