In this study, a careful examination was conducted to analyse the actin and microtubule (MT) cytoskeleton organisation during Drosophila oogenesis. We found that at stage 9/10a the actin cytoskeleton at the oocyte cortex is assembled into long bundles, which are essential for anchoring the MT minus-ends at the cortex. The formation of actin bundles requires the function of Profilin. Capu and Spire act downstream of the bundle formation, most likely by anchoring MT minus-ends at the cortex by crosslinking F-actin and MTs. At stage 10b, the actin bundles disassemble and the MT minus-ends are relocated from the actin cortex to subcortical regions. Subsequently, fast ooplasmic streaming is initiated and MTs form parallel arrays at subcortical regions. To identify the regulators of the organisation of the oocyte cytoskeleton, a mutation in a serine/threonine kinase Tao-1, Tao-1No.7 was generated. The analysis of Tao-1No.7 mutants revealed a novel phenotype for the cytoskeleton organisation of the oocyte. In Tao-1No.7 mutant oocytes the cortical actin bundling is disrupted. Unlike in other mutants which affect actin bundling, in Tao-1No.7 oocytes MTs are not forming parallel arrays at subcortical regions; but show high MT density within the entire ooplasm. Thus, the MT network is completely disrupted in Tao-1No.7 oocytes. As a result, the transcripts for the axis determinants are not transported to correct subcellular locations, and as a consequence the embryonic axis is not properly established. The oogenesis phenotypes observed in Tao-1No.7 mutants was rescued by the expression of a Tao-1 cDNA, verifying that Tao-1No.7 is an allele of Tao-1. Nevertheless, a deletion removing the Tao-1 locus completely does not exhibit the defects in the cytoskeletal organisation of the oocyte. Therefore, Tao-1No.7 is most likely a gain of function allele of Tao-1, which shows a phenotype only in a homozygous situation (recessive gain of function)
