Maternal gametes and epigenetic inheritance

Iovino Lab

Ova are generated by oogenesis in the female germline, the ovary. During the differentiation process, their chromatin undergoes profound condensation, transcriptional shutdown and reductive division to haploidy. Defects in any of these processes can lead to full sterility with complete lack of functional gametes.

Figure 1 WT ovariole showing that H3K27me3, a PTM associated with PRC2, is specifically retained in the oocyte (arrow) and not in the nurse cells (arrowhead). — **Figure 1** WT ovariole showing that H3K27me3, a PTM associated with PRC2, is specifically retained in the oocyte (arrow) and not in the nurse cells (arrowhead).

**Figure 1** WT ovariole showing that H3K27me3, a PTM associated with PRC2, is specifically retained in the oocyte (arrow) and not in the nurse cells (arrowhead).

Chromatin condensation and transcriptional shut down in the ovum are mainly achieved trough epigenetic mechanisms. Mutations in epigenetic modifiers affecting methylation of histone 3 at lysine 9 (H3K9) and at lysine 4 (H3K4) have been shown to cause defects in fertility in vertebrate and invertebrates. We have recently identified the Polycomb Repressive Complex 2 (PRC2) as a critical chromatin determinant of Drosophila oocyte cell fate (Figure 1). PRC2 is the major complex that catalyzes trimethylation of histone 3 at lysine 27 (H3K27me3), a mark usually associated with facultative heterochromatin and transcriptional repression (Figure 2). In the absence of PRC2 components, the oocyte undergoes a trans-determination process and becomes a polyploid cell. The resulting lack of a functional haploid gamete causes full sterility. Our lab is now currently exploring the role of this complex in controlling post-meiotic gametes transcription and its role in fertilization.