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The retention of particular genes after the whole genome duplication in zebrafish has given insights into how genes may evolve through partitioning of ancestral functions. We examine the partitioning of expression patterns and functions of two zebrafish  kit ligands, kit ligand a (kitla)  and  kit ligand b (kitlb),  and discuss their possible coevolution with the duplicated zebrafish  kit  receptors  (kita  and  kitb).  In situ hybridizations show that  kitla  mRNA is expressed in the trunk adjacent to the notochord in the middle of each somite during stages of melanocyte migration and later expressed in the skin, when the receptor is required for melanocyte survival.  kitla  is also expressed in other regions complementary to  kita  receptor expression, including the pineal gland, tail bud, and ear. In contrast,  kitlb  mRNA is expressed in brain ventricles, ear, and cardinal vein plexus, in regions generally not complementary to either zebrafish  kit  receptor ortholog. However, like  kitla, kitlb  is expressed in the skin during stages consistent with melanocyte survival. Thus, it appears that  kita  and  kitla  have maintained congruent expression patterns, while  kitb  and  kitlb  have evolved divergent expression patterns. We demonstrate the interaction of  kita  and  kitla  by morpholino knockdown analysis.  kitla  morphants, but not  kitlb  morphants, phenocopy the null allele of  kita,  with defects for both melanocyte migration and survival. Furthermore,  kitla  morpholino, but not  kitlb  morpholino, interacts genetically with a sensitized allele of  kita,  confirming that  kitla  is the functional ligand to  kita.  Last, we examine  kitla  overexpression in embryos, which results in hyperpigmentation caused by an increase in the number and size of melanocytes. This hyperpigmentation is dependent on  kita  function. We conclude that following genome duplication,  kita  and  kitla  have maintained their receptor–ligand relationship, coevolved complementary expression patterns, and that functional analysis reveals that most or all of the  kita  receptor's function in the embryo are promoted by its interaction with  kitla.

Gene Duplication of the Zebrafish kit ligand and Partitioning of Melanocyte Development Functions to kit ligand a