| Literature DB >> 27918537 |
Changwei Shao1,2, Baolong Bao3, Zhiyuan Xie4, Xinye Chen3, Bo Li4, Xiaodong Jia1,2, Qiulin Yao4, Guillermo Ortí5, Wenhui Li4, Xihong Li1,2, Kristin Hamre6,7, Juan Xu3, Lei Wang1,2, Fangyuan Chen4, Yongsheng Tian1,2, Alex M Schreiber8, Na Wang1,2, Fen Wei3, Jilin Zhang4, Zhongdian Dong1,2, Lei Gao3, Junwei Gai3, Takashi Sakamoto9, Sudong Mo1,2, Wenjun Chen3, Qiong Shi4, Hui Li3, Yunji Xiu1,2, Yangzhen Li1,2, Wenteng Xu1,2, Zhiyi Shi3, Guojie Zhang4, Deborah M Power10,11, Qingyin Wang1,2, Manfred Schartl12,13, Songlin Chen1,2.
Abstract
Flatfish have the most extreme asymmetric body morphology of vertebrates. During metamorphosis, one eye migrates to the contralateral side of the skull, and this migration is accompanied by extensive craniofacial transformations and simultaneous development of lopsided body pigmentation. The evolution of this developmental and physiological innovation remains enigmatic. Comparative genomics of two flatfish and transcriptomic analyses during metamorphosis point to a role for thyroid hormone and retinoic acid signaling, as well as phototransduction pathways. We demonstrate that retinoic acid is critical in establishing asymmetric pigmentation and, via cross-talk with thyroid hormones, in modulating eye migration. The unexpected expression of the visual opsins from the phototransduction pathway in the skin translates illumination differences and generates retinoic acid gradients that underlie the generation of asymmetry. Identifying the genetic underpinning of this unique developmental process answers long-standing questions about the evolutionary origin of asymmetry, but it also provides insight into the mechanisms that control body shape in vertebrates.Entities:
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Year: 2016 PMID： 27918537 DOI： 10.1038/ng.3732
Source DB: PubMed Journal: Nat Genet ISSN： 1061-4036 Impact factor: 38.330