Derepression of transposable elements (TEs) in the course of epigenetic 
reprogramming of the mouse embryonic germline necessitates the existence of a 
robust defense that is comprised of PIWI/piRNA pathway and de novo DNA 
methylation machinery. To gain further insight into biogenesis and function of 
piRNAs, we studied the intracellular localization of piRNA pathway components 
and used the combination of genetic, molecular, and cell biological approaches 
to examine the performance of the piRNA pathway in germ cells of mice lacking 
Maelstrom (MAEL), an evolutionarily conserved protein implicated in transposon 
silencing in fruit flies and mice. Here we show that principal components of the 
fetal piRNA pathway, MILI and MIWI2 proteins, localize to two distinct types of 
germinal cytoplasmic granules and exhibit differential association with 
components of the mRNA degradation/translational repression machinery. The first 
type of granules, pi-bodies, contains the MILI-TDRD1 module of the piRNA pathway 
and is likely equivalent to the enigmatic "cementing material" first described 
in electron micrographs of rat gonocytes over 35 years ago. The second type of 
granules, piP-bodies, harbors the MIWI2-TDRD9-MAEL module of the piRNA pathway 
and signature components of P-bodies, GW182, DCP1a, DDX6/p54, and XRN1 proteins. 
piP-bodies are found predominantly in the proximity of pi-bodies and the two 
frequently share mouse VASA homolog (MVH) protein, an RNA helicase. In 
Mael-mutant gonocytes, MIWI2, TDRD9, and MVH are lost from piP-bodies, whereas 
no effects on pi-body composition are observed. Further analysis revealed that 
MAEL appears to specifically facilitate MIWI2-dependent aspects of the piRNA 
pathway including biogenesis of secondary piRNAs, de novo DNA methylation, and 
efficient downregulation of TEs. Cumulatively, our data reveal elaborate 
cytoplasmic compartmentalization of the fetal piRNA pathway that relies on MAEL 
function.