Evolution of Shh endoderm enhancers during morphological transition from ventral lungs to dorsal gas bladder

Tomoko Sagai, Takanori Amano, Akiteru Maeno, Tetsuaki Kimura, Masatoshi Nakamoto, Yusuke Takehana, Kiyoshi Naruse, Norihiro Okada, Hiroshi Kiyonari and Toshihiko Shiroishi ()
Additional contact information
Tomoko Sagai: Mammalian Genetics Laboratory, Genetic Strains Research Center, National Institute of Genetics
Takanori Amano: Mammalian Genetics Laboratory, Genetic Strains Research Center, National Institute of Genetics
Akiteru Maeno: Mammalian Genetics Laboratory, Genetic Strains Research Center, National Institute of Genetics
Tetsuaki Kimura: Interuniversity Bio-Backup Project Center, National Institute for Basic Biology
Masatoshi Nakamoto: Interuniversity Bio-Backup Project Center, National Institute for Basic Biology
Yusuke Takehana: Interuniversity Bio-Backup Project Center, National Institute for Basic Biology
Kiyoshi Naruse: Interuniversity Bio-Backup Project Center, National Institute for Basic Biology
Norihiro Okada: National Cheng Kung University
Hiroshi Kiyonari: Laboratory for Animal Resources and Genetic Engineering, RIKEN Center for Developmental Biology (CDB)
Toshihiko Shiroishi: Mammalian Genetics Laboratory, Genetic Strains Research Center, National Institute of Genetics

Nature Communications, 2017, vol. 8, issue 1, 1-12

Abstract: Abstract Shh signalling plays a crucial role for endoderm development. A Shh endoderm enhancer, MACS1, is well conserved across terrestrial animals with lungs. Here, we first show that eliminating mouse MACS1 causes severe defects in laryngeal development, indicating that MACS1-directed Shh signalling is indispensable for respiratory organogenesis. Extensive phylogenetic analyses revealed that MACS1 emerged prior to the divergence of cartilaginous and bony fishes, and even euteleost fishes have a MACS1 orthologue. Meanwhile, ray-finned fishes evolved a novel conserved non-coding sequence in the neighbouring region. Transgenic assays showed that MACS1 drives reporter expression ventrally in laryngeal epithelium. This activity has been lost in the euteleost lineage, and instead, the conserved non-coding sequence of euteleosts acquired an enhancer activity to elicit dorsal epithelial expression in the posterior pharynx and oesophagus. These results implicate that evolution of these two enhancers is relevant to the morphological transition from ventral lungs to dorsal gas bladder.

Date: 2017
References: Add references at CitEc
Citations:

Downloads: (external link)
https://www.nature.com/articles/ncomms14300 Abstract (text/html)

Related works:
This item may be available elsewhere in EconPapers: Search for items with the same title.

Export reference: BibTeX RIS (EndNote, ProCite, RefMan) HTML/Text

Persistent link: https://EconPapers.repec.org/RePEc:nat:natcom:v:8:y:2017:i:1:d:10.1038_ncomms14300

Ordering information: This journal article can be ordered from
https://www.nature.com/ncomms/

DOI: 10.1038/ncomms14300

Access Statistics for this article

Nature Communications is currently edited by Nathalie Le Bot, Enda Bergin and Fiona Gillespie

More articles in Nature Communications from Nature
Bibliographic data for series maintained by Sonal Shukla () and Springer Nature Abstracting and Indexing ().