Although progress has been made in resolving the genetic pathways that specify neuronal asymmetries in the brain, little is
known about genes that mediate the development of structural asymmetries between neurons on left and right. In this study,
we identify daam1a as an asymmetric component of the signalling pathways leading to asymmetric morphogenesis of the habenulae in zebrafish.
Daam1a is a member of the Formin family of actin-binding proteins and the extent of Daam1a expression in habenular neuron
dendrites mirrors the asymmetric growth of habenular neuropil between left and right. Local loss and gain of Daam1a function
affects neither cell number nor subtype organisation but leads to a decrease or increase of neuropil, respectively. Daam1a
therefore plays a key role in the asymmetric growth of habenular neuropil downstream of the pathways that specify asymmetric
cellular domains in the habenulae. In addition, Daam1a mediates the development of habenular efferent connectivity as local
loss and gain of Daam1a function impairs or enhances, respectively, the growth of habenular neuron terminals in the interpeduncular
nucleus. Abrogation of Daam1a disrupts the growth of both dendritic and axonal processes and results in disorganised filamentous
actin and α-tubulin. Our results indicate that Daam1a plays a key role in asymmetric habenular morphogenesis mediating the
growth of dendritic and axonal processes in dorsal habenular neurons.