Yet another function for kinesin.

The establishment of the Drosophila body structure is determined in part by the localization of morphogenetic factors during embryogenesis. One common mechanism for localizing such morphogens is the transport of their mRNAs to sites of action within the developing oocyte. Then, translation of the localized mRNA molecule leads to the concentration of nascent protein in the proper region of the developing fly.For instance, localization of the oskar mRNA to the posterior pole of the Drosophila oocyte is required for patterning the posterior structures of the fly. Moreover, it has been shown that Staufen, a protein that migrates to the posterior pole during embryogenesis (stage 9), can bind to oskar mRNA and is required for its accumulation in the posterior of the oocyte. The use of microtubule-disrupting drugs, which prevent the posterior localization of oskar mRNA during oogenesis, had hinted that some form of microtubule-based transport probably underlies mRNA transport during development of the fly oocyte.Now, work by Brendza et al. has implicated the plus-end-directed microtubule motor kinesin in this process 1xA function for kinesin I in the posterior transport of oskar mRNA and Staufen protein. Brendza, R.P. et al. Science. 2000; 289: 2120–2122Crossref | PubMed | Scopus (231)See all References1. To do so, they generated mutant flies in which female germ-line cells lacked the kinesin heavy chain (Khc) gene. When those females were mated to wild-type males, embryogenesis failed in either the blastoderm or early gastrula stages. In those embryos that had reached the blastoderm stage, there was a lack of posterior pole cells. Consistent with the defect in posteriorization, both the Staufen protein and oskar mRNA failed to accumulate at the posterior pole of the embryo. Notably, the loss of Khc did not cause general defects in mRNA localization as the mutant embryos were able to properly localize the bicoid mRNA at the anterior pole. Moreover, loss of kinesin function did not cause a general loss of microtubule structures in the mutant embryos. Thus, kinesin is required for transporting the Staufen/oskar complex to the posterior of the embryo during development.These observations are consistent with the previous observation that microtubule plus-ends are concentrated at the posterior pole of the embryo during stages 8–9 (when oskar becomes localized). The finding that a plus-end-directed motor is required for localizing oskar mRNA suggests that a complex consisting of kinesin, staufen and oskar moves along the polarized microtubules to the posterior of the embryo. However, the authors were unable to detect a biochemical interaction between KHC and Staufen by immunoprecipitation. Thus, kinesin might be interacting with vesicles that contain the Staufen/oskar complexes rather than directly binding to the protein–mRNA complex. Alternatively, the authors suggest that kinesin might localize other proteins that are required for transport of Staufen/oskar to the cortex of the oocyte. As such, a characterization of the mechanism by which kinesin elicits mRNA localization in Drosophila will certainly shed some light on the process by which microtubule-based motors contribute to development of multicellular organisms.