Abstract
Dendritic arbors of different neuronal subtypes cover distinct spatial territories, known as dendritic fields, to receive specific inputs in a nervous system. How the size of dendritic fields is determined by cell-intrinsic factors during development remains primarily unknown. To address this issue, we used the Drosophila embryonic peripheral nervous system. In each hemisegment, six dorsal cluster dendritic arborization (DA) neurons elaborate stereotypic dendritic branching patterns underneath the epidermis. Here we report the identification of loss-of-function mutations in the tropomyosin II gene (TmII) that result in expanded dendritic fields of DA neurons. Mosaic analysis with a repressible cell marker demonstrated that TmII functions in a cell-autonomous manner to control the formation of dendritic fields. Furthermore, we show that TmII genetically interacted with flamingo, a gene encoding a membrane receptor-like molecule that affects dendritic growth. TmII encodes multiple isoforms of a protein that stabilizes actin filaments. Our findings suggest that tropomyosin helps control the size of dendritic fields by regulating actin cytoskeletal dynamics.
