Figure 7.

Mutation of Kctd12 proteins leads to excess Hb neuropil. A, By 4 dpf, WT larvae display elaborate extension of neuropil in both Hb and express both Kctd12.1 and 12.2 (green, inset). B, The kctd12.1 coding sequence is disrupted by a large viral insertion in kctd12.1^vu442 mutants (note lack of Kctd12.1 staining in lateral subnuclei in inset). Hb neuropil in Kctd12.1-negative larvae is slightly expanded in lateral subnuclei. C, An ENU-induced stop codon in the coding sequence of kctd12.2 in kctd12.2^fh312 mutants leads to loss of Kctd12.2 protein expression (note lack of Kctd12.2 staining in medial subnuclei in inset). Kctd12.2-negative larvae also display excess elaboration of Hb neuropil, particularly in the medial subnuclei. D, kctd12.1^vu442; kctd12.2^fh312 double mutants are negative for both Kctd12 proteins (green, inset), and Hb neuropil is expanded in both the lateral and medial subnuclei. E, Volumetric quantification of neuropil expansion in kctd12 mutants. Neuropil expansion is restricted to lateral subnuclei in Kctd12.1-negative larvae, consistent with the expression pattern of Kctd12.1. Neuropil expansion in Kctd12.2-negative larvae affects medial subnuclei as well as the right lateral subnucleus. Double mutant larvae display neuropil expansion in all subnuclei (asterisks indicate statistical difference compared with WT). Scale bars, 50 μm. *p < 0.05, **p < 0.01, two-tailed test.