Transposons are predominantly expressed in the germline because of their interest in trans-generational inheritance. However, a class of retro-transposons have evolved in Drosophila species that homed in the somatic compartment of female gonad to infect the germline cells. The piRNA pathway actively silences the expression of these retro-transposons and the loss of piRNA pathway in the somatic cells causes deleterious effects in ovarian development. The causative molecular defects are not known whether the phenotype is caused by transposon over-expression or by unknown mechanisms. We entertain the hypothesis that the transposon defence mechanism that took care of the invasion of retro-transposons is repurposed to play a role in the development of non-germline cells in the gonad. We aim to anatomically and molecularly identify the causative defects in the somatic development of piRNA pathway mutant ovaries.
Techniques involved: Drosophila genetics; various Gal4 drivers, RNAi lines, GFP and lacZ markers, immuno-histochemistry, and RNA-sequencing.