Recent studies have suggested that PIWI proteins in sea urchin (Seawi) and Xenopus (Xiwi) can interact with the MTs of the meiotic spindle, while fly ovarioles with mutations in any of several piRNA pathway genes, including spn-E, aub, and armi, have disorganized MTs. PIWI proteins function in transposon silencing via association with piRNAs and maintain genome integrity during germline development. The findings that γTub does not accumulate at centrosomes in the mael germarium and is ectopically expressed in the mael egg chamber suggest that Mael regulates localization of γTub at centrosomes through its complex formation and is thereby involved in properly organizing or positioning the MTOC (Sato, 2011). It was hypothesized that reduced activity of γTub could activate the oocyte determination program in one of the nurse cells by ectopically presenting MTOC material. γTub is involved in the nucleation of MTs and is present in the centrosomes and MTOCs in many different systems. These γTub mutant defects are very similar to those found in mael mutants in this study. A previous report has shown that weaker mutant alleles of γTub affect the number of nurse cells and oocytes within the egg chamber. The simplest hypothesis is that Mael might serve as a platform that nucleates other MTOC components to form a functional MTOC. Currently, the detailed mechanism by which Mael functions in MT organization is not clear.

γTub does not migrate to a developing oocyte in mael germariums, suggesting that Mael is required for the migration of centrioles from the cytoplasm of cysts to pro-oocytes in the germarium. Mael is concentrated in the centrosomal region and is colocalized with αTub and γTub during cyst cell divisions. Initial polarization of the oocyte during the oocyte specification phase in the germarium requires replacement of the fusome by a polarized MT network, which correlates with the formation of the MTOC. These results indicate that Mael specifically regulates MTOC formation, and thereby plays a key role in coordinating dynamic MT organization during Drosophila oogenesis (Sato, 2011). It was also observed that loss of mael affects the number and position of the oocytes in egg chambers and induces fusion of egg chambers. In this study, it was shown that Mael is an MTOC component and that dynamic organization of MTs does not occur in developing mael oocytes, which correlates with mislocalization of other MTOC components. These findings suggest a model in which Mael serves as a platform that nucleates other MTOC components to form a functional MTOC in early oocyte development, which is independent of Chk2 activation and DNA damage signaling (Sato, 2011). Finally, this study shows that the axis specification defects in mael mutants are not suppressed by a mutation in mnk, which encodes a Chk2 homolog. During oogenesis, the loss of mael affects oocyte determination and induces egg chamber fusion. MTOC components mislocalize in mael mutant germarium and egg chambers, leading to centrosome migration defects. Mael colocalizes with αTubulin and γTubulin to centrosomes in dividing cyst cells and follicle cells. Mael forms complexes with microtubule-organizing center (MTOC) components, including Centrosomin, Mini spindles, and γTubulin. A piRNA pathway gene, maelstrom (mael), is critical for the establishment of oocyte polarity in the developing egg chamber during Drosophila oogenesis. This results from the activation of the DNA damage checkpoint factor Checkpoint kinase 2 (Chk2) due to transposon derepression. Mutations in Drosophila PIWI-interacting RNA (piRNA) pathway genes often disrupt the axes of the oocyte. The establishment of body axes in multicellular organisms requires accurate control of microtubule polarization.

Maelstrom coordinates microtubule organization during Drosophila oogenesis through interaction with components of the MTOC

Niche maelstrom