A small set of conserved genes, including sp5 and Hox, are activated by Wnt signaling in the posterior of planarians and acoels
Name
journal.pgen.1008401.pdf
Description
Published version
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7.31 MB
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Checksum (MD5)
eec109a6e4f12ef5ef9a3a0436152a4b
Author(s)
Tewari, Aneesha G.
Owen, Jared H.
Petersen, Christian P.
Wagner, Daniel E.
Reddien, Peter W.
Date Issued
October 2019
Journal
PLOS genetics
Publisher
Public Library of Science (PLoS)
Citation
Tewari, Aneesha G. et al. “A small set of conserved genes, including sp5 and Hox, are activated by Wnt signaling in the posterior of planarians and acoels.” PLOS genetics 15 (2019): e1008401 © 2019 The Author(s)
Version
Final published version
Abstract
Wnt signaling regulates primary body axis formation across the Metazoa, with high Wnt signaling specifying posterior identity. Whether a common Wnt-driven transcriptional program accomplishes this broad role is poorly understood. We identified genes acutely affected after Wnt signaling inhibition in the posterior of two regenerative species, the planarian Schmidtea mediterranea and the acoel Hofstenia miamia, which are separated by >550 million years of evolution. Wnt signaling was found to maintain positional information in muscle and regional gene expression in multiple differentiated cell types. sp5, Hox genes, and Wnt pathway components are down-regulated rapidly after β-catenin RNAi in both species. Brachyury, a vertebrate Wnt target, also displays Wnt-dependent expression in Hofstenia. sp5 inhibits trunk gene expression in the tail of planarians and acoels, promoting separate tail-trunk body domains. A planarian posterior Hox gene, Post-2d, promotes normal tail regeneration. We propose that common regulation of a small gene set–Hox, sp5, and Brachyury–might underlie the widespread utilization of Wnt signaling in primary axis patterning across the Bilateria.
MIT Department
Whitehead Institute for Biomedical Research
Massachusetts Institute of Technology. Department of Biology
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Creative Commons Attribution 4.0 International license
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DOI of Published Version
https://doi.org/10.1371/journal.pgen.1008401
