Table 2.

the flamenco story

Much of what we know today on the piRNA pathway was discovered using the Drosophila model. Especially, a considerable effort started 40 years ago in D. melanogaster led to the early discovery of a gene producing piRNAs and silencing Gypsy in a piwi dependent manner (see [199] for a review). This gene named flamenco was the first piRNA cluster identified. In the 1980s, the ovoD dominant mutation was identified in D. melanogaster and associated with female sterility [200]. Interestingly, crosses between ovoD males and females from a particular strain led to the reversion of the phenotype and the recovery of fertility of the daughters, in addition to numerous mutations at other loci. Further work revealed that the particular strain used for the mothers actually displayed high copy numbers of uncontrolled Gypsy, whose transposition into ovo led to a null allele and reversion of sterility [201]. And then, it was demonstrated that the locus controlling Gypsy activity was the flamenco locus, located on the X chromosome and containing a lot of TE sequences [202, 203]. In 2004, Sarot and collaborators found out that Gypsy transposition was sensitive to a mutation in piwi, a gene known to affect RNA-mediated silencing [204]. They also demonstrated that small RNAs homologous to Gypsy where present in silenced tissues. For the first time a gene producing small RNAs was associated with TE silencing, and Piwi was implicated in this process. Despite the subsequent discovery of many other piRNA clusters in D. melanogaster, flamenco is still widely studied as a model and produces most of the piRNAs in ovarian somatic cells [197, 205–207].