Meeting Abstract
51.3 Sunday, Jan. 5 10:45 Differential Activity of SoxE Transcription Factors in Neural Crest Development and Evolution MCCAULEY, DW*; LEE, E; YUAN, T; NGUYEN, K; Univ. of Oklahoma, Norman; Univ. of Oklahoma, Norman; Univ. of Oklahoma, Norman; Univ. of Oklahoma, Norman dwmccauley@ou.edu
SoxE genes arose by duplication and are key regulators of neural crest cell (NCC) development. Sea lampreys are primitive vertebrates and also possess three SoxE genes, all expressed in neural crest. In order to address how gene duplication has influenced their roles, we examined the ability of lamprey SoxE genes to regulate NCC differentiation in zebrafish lacking expression of Sox9a and Sox10. Lamprey SoxE genes are able to rescue the differentiation of melanogenesis and neurogenesis in zebrafish Sox10 mutants. The lamprey Sox9 ortholog, PmSoxE3, was unable to promote cartilage differentiation in zebrafish Sox9a mutants. Surprisingly, lamprey-specific PmSoxE1, was able to promote the differentiation of small cartilage nodules in Sox9a mutants. Our data suggest an early SoxE gene already possessed melanogenic, neurogenic and chondrogenic regulatory capabilities prior to gene duplication. Further, melanogenic and neurogenic activities were partitioned to SoxE2 in lampreys and Sox10in jawed vertebrates, whereas the chondrogenic role was partitioned to Sox9 in gnathostomes but to SoxE1 in lampreys. Morphogenesis of pigment cells and neurons in Sox10 mutants rescued by heterospecific SoxE expression appeared normal, but PmSoxE1 did not rescue morphogenesis of the craniofacial skeleton in Sox9a mutants. This result suggests lamprey SoxE genes may lack the regulatory ability to direct morphogenesis of the gnathostome craniofacial skeleton. We speculate that the lamprey Sox9 gene, SoxE3, acquired lamprey-specific roles in cartilage morphogenesis through neofunctionalization. Our study demonstrates the differential adaptation and specialization of SoxE proteins across the agnathan-gnathostome boundary, and reveals that phylogenetic signal is not always a reliable predictor of functional conservation.
