In Drosophila, the asymmetric cell division of embryonic neuroblasts requires, among other things, the formation of a basal crescent-shaped complex by cell-fate determinants and their adaptor proteins, one of which is Miranda. Because Miranda is localized to the apical cortex before the basal crescent forms, Yuh Nung Jan and colleagues figured that Miranda might require a motor protein that targets it to the basal site. Now they've found one — myosin VI Jaguar (Jar) — according to a report in Developmental Cell.

The Jan laboratory isolated Miranda-containing protein complexes from fly embryos using anti-Miranda antibodies and identified myosin II Zipper (Zip), which negatively regulates basal transport of Miranda, and Jar. Jar binding to Miranda is direct, as shown in glutathione S- transferase (GST) pull-down studies.

So what's the functional significance of this interaction? To address this question, Jan and co-workers took three independent approaches to reduce Jar activity in neuroblasts. In all cases, reduced Jar activity resulted in mislocalization of Miranda and misorientation of mitotic spindles — spindle reorientation being another feature of asymmetric neuroblast cell division.

Double-mutant studies indicated that Jar functions synergistically with Lethal giant larvae (Lgl), which is known to be required for basal-crescent formation. The apical complex was not affected, which led the authors to conclude that Jar and Lgl function downstream of, or in parallel to, apical localization.

All the myosins previously implicated in asymmetric cell division (including Zip in fly, as well as the ones in worm and yeast) are barbed-end-directed myosins, which move towards the plus ends of actin filaments. Jar is the first pointed-end-directed myosin. No doubt, future studies will be aimed at uncovering the mechanism by which Jar mediates basal targeting and spindle reorientation.