Further analysis on the molecular nature of the drop out locus has revealed that in contrast to the report in Meyer et al 2006 (FBrf0194224), drop out is not allelic to argonaute 2 (ago2). This conclusion is supported by the following findings: (1) Only recently mRNA null mutations of ago2 became available. Those alleles fully complement dop mutant alleles. (2) The molecular lesions of dop alleles were reported (FBrf0194224) to represent in frame deletions of glutamine rich repeats (GRR) in the amino-terminus of the Ago2 protein. By comparing 24 different D. melanogaster haplotypes we discovered that the amino-terminal domain of Ago2 is highly variable and that the alteration in the amino-terminal GRR pattern observed in the dop46 allele is not unique. (3) The GRR haplotype of dop46 is not the cause of the developmental phenotype of embryos derived from homozygous dop mutant mothers. A D.melanogaster strain with the identical GRR haplotype does not exhibit gross developmental defects. We conclude that ago2 and dop are different genes. An account of these data will be submitted for publication soon.
