Knight Robert D, Javidan Yashar, Nelson Sarah, Zhang Tailin, Schilling Thomas
Department of Developmental and Cell Biology, University of California, Irvine, California, USA.
Dev Dyn. 2004 Jan;229(1):87-98. doi: 10.1002/dvdy.10494.
Members of the AP-2 transcription factor family have critical roles in many aspects of embryonic development. The zebrafish tfap2a mutant lockjaw (low) displays defects in skeletal and pigment cell derivatives of the neural crest. Here we show essential roles for tfap2a in subsets of embryonic cartilages and pigment cells. Defects in cartilage of the hyoid arch in low correlate with a loss of Hox group 2 gene expression and are suggestive of a transformation to a mandibular fate. In contrast, loss of joints in the mandibular arch and defects in certain types of pigment cells suggest a requirement for tfap2a independent of Hox regulation. Early melanophores do not develop in low mutants, and we propose that this results in part from a loss of kit function, leading to defects in migration, as well as kit-independent defects in melanophore specification. Iridophores are also reduced in low, in contrast to xanthophores, revealing a role for tfap2a in the development of pigment subpopulations. We propose a model of tfap2a function in the neural crest in which there are independent functions for tfap2a in specification of subpopulations of pigment cells and segmental patterning of the pharyngeal skeleton through the regulation of Hox genes. Developmental Dynamics 229:87-98, 2004.
AP-2转录因子家族成员在胚胎发育的许多方面都起着关键作用。斑马鱼tfap2a突变体“锁颌”（low）在神经嵴的骨骼和色素细胞衍生物中表现出缺陷。在此我们展示了tfap2a在胚胎软骨和色素细胞亚群中的重要作用。low中舌弓软骨的缺陷与Hox 2基因表达的缺失相关，并提示向下颌命运的转变。相比之下，下颌弓关节的缺失和某些类型色素细胞的缺陷表明tfap2a的需求独立于Hox调控。早期黑素细胞在low突变体中不发育，我们认为这部分是由于kit功能的丧失，导致迁移缺陷，以及黑素细胞特化中与kit无关的缺陷。与黄色素细胞相反，反光色素细胞在low中也减少，揭示了tfap2a在色素亚群发育中的作用。我们提出了一个tfap2a在神经嵴中的功能模型，其中tfap2a在色素细胞亚群的特化以及通过Hox基因调控咽骨骼的节段模式中具有独立功能。《发育动力学》229:87 - 98，2004年。
