RT Journal Article SR Electronic T1 Asymmetric Inhibition of Ulk2 Causes Left–Right Differences in Habenular Neuropil Formation JF The Journal of Neuroscience JO J. Neurosci. FD Society for Neuroscience SP 9869 OP 9878 DO 10.1523/JNEUROSCI.0435-11.2011 VO 31 IS 27 A1 Robert W. Taylor A1 Jenny Y. Qi A1 Anna K. Talaga A1 Taylur P. Ma A1 Luyuan Pan A1 Clinton R. Bartholomew A1 Daniel J. Klionsky A1 Cecilia B. Moens A1 Joshua T. Gamse YR 2011 UL http://www.jneurosci.org/content/31/27/9869.abstract AB Studies of the zebrafish epithalamus have provided recent insights into the development of left–right brain asymmetry, which is crucial to normal human brain function. The habenular nuclei of zebrafish are robustly asymmetric, with dense elaboration of neuropil only in the left lateral subnucleus. Because this feature is tightly correlated with asymmetric expression of K+ channel tetramerization domain-containing proteins 12.1 and 12.2 (Kctd12.1/12.2), we screened for Kctd12.1-interacting proteins to identify molecular mechanisms leading to neuropil asymmetry, and uncovered a novel interaction between Kctd12.1 and Unc-51-like kinase 2 (Ulk2). We show here that knockdown of Ulk2 or overexpression of Kctd12 proteins reduces asymmetric neuropil elaboration. Conversely, overexpression of Ulk2 or mutation of kctd12 genes causes excess neuropil elaboration. We conclude that Ulk2 activity promotes neuropil elaboration while Kctd12 proteins limit Ulk2 activity asymmetrically. This work describes a regulatory mechanism for neuronal process extension that may be conserved in other developmental contexts in addition to the epithalamus.