![]() However, key F-actin regulators in dendrites that contribute to where and how branches are spatially organized remain unclear, particularly in vivo, where arbors grow within their native cellular context. Cellular F-actin is known to be assembled from actin monomers by a range of proteins that nucleate filaments, regulate their elongation and turnover, and crosslink them into networks or bundles ( Pollard and Cooper, 2009). In addition, F-actin is the major constituent of dendritic filopodia, finger-like projections that initiate branch outgrowth. F-actin and MTs are major structural components of dendrites that support the transport by motor proteins of organelles and macromolecular complexes that are used to build and maintain arbors. ![]() ![]() However, it remains largely unknown how they influence the dynamic remodeling of the dendritic cytoskeleton that accompanies branching and outgrowth, as scant progress has been made in linking these transcription factors to key effectors that control rearrangements of actin filaments (F-actin) and microtubules (MTs). Intrinsic control by transcription factors has emerged as an important mechanism that regulates the branching patterns of dendrites ( Parrish et al., 2006 Ou et al., 2008 Jan and Jan, 2010 Smith et al., 2010 de la Torre-Ubieta and Bonni, 2011). We conclude that the Lola-Spir pathway is crucial for the spatial arrangement of branches within dendritic trees and for neural circuit function because it provides balanced control of the F-actin cytoskeleton. Removal of Spir from class IV da neurons reduced F-actin levels and total branch number, shifted the position of greatest branch density away from the cell soma, and compromised nocifensive behavior. We found Spir to be expressed in dendritic arbors and to be important for their development. Thus, an important role of Lola is to limit expression of Spir to appropriate levels within da neurons. The increased Spir expression contributed to the abnormal F-actin-rich dendrites and the decreased nocifensive responses because both were suppressed by reduced dose of Spir. Selective removal of Lola from only class IV da neurons decreased the evasive responses of larvae to nociception. Loss of Lola from da neurons reduced the overall length of dendritic arbors, increased the expression of Spir, and produced inappropriate F-actin-rich dendrites at positions too near the cell soma. Here, we describe a cell-intrinsic pathway sculpting dendritic arborization (da) neurons in Drosophila that requires Longitudinals Lacking (Lola), a BTB/POZ transcription factor, and its control of the F-actin cytoskeleton through Spire (Spir), an actin nucleation protein. The architectures of dendritic trees are crucial for the wiring and function of neuronal circuits because they determine coverage of receptive territories, as well as the nature and strength of sensory or synaptic inputs.
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