 During brain development, neurons form a unique, tree-like pattern of dendrites that fits their specific function. New dendritic branches are stabilized by microtubules, which establish the internal structure of cells. However, too much or too little dendritic branching can produce improper neuronal connections, resulting in neuronal dysfunction that can lead to intellectual disability or psychiatric illness. This study found that the branching pattern of neurons is determined by a set of proteins that organize microtubules. The researchers used fruit flies to examine how the dendritic branching process is controlled. In searching for factors that might affect the formation of dendrite-stabilizing microtubules, they found that the transcription factor abrupt restricts dendritic branching by changing the arrangement of microtubules. In fruit fly neurons, abrupt induce the production of microtubule-related proteins, in particular centrosomen, the same protein that helps cells to properly separate their chromosomes during cell division. In the dendritic tree, centrosomen clustered along dendritic branches, especially at branch points and at the tips of branches. At these sites, centrosomen bound to the Golgi apparatus, which acts as a foundation for the microtubule network. In the presence of centrosomen and abrupt, new microtubules grew away from the Golgi apparatus in the same direction, preventing them from pushing outward into new dendrites. However, eliminating centrosomen function prevented abrupt from restricting dendritic branching, leading to excessive dendrite formation. This occurred because without centrosomen, microtubules were free to push out in any direction, thereby forming new dendrites. Taken together, these findings revealed that centrosomen limits dendritic branching during neuronal development by inhibiting the formation of stabilizing microtubules in newly formed dendrites. This new understanding of the function of centrosomen helps to explain how dendritic trees with different complexities are formed. Further studies are needed to determine whether dendrite branching patterns are altered in humans with centrosomen mutations, and whether interventions targeting dendrite formation processes might protect against the onset of some neurological disorders.