Functional divergence of paralogous transcription factors supported the evolution of biomineralization in echinoderms

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Abstract

Alx1 is a pivotal transcription factor in a gene regulatory network that controls skeletogenesis throughout the echinoderm phylum. We performed a structure-function analysis of sea urchin Alx1 using a rescue assay and identified a novel, conserved motif (Domain 2) essential for skeletogenic function. The paralogue of Alx1, Alx4, was not functionally interchangeable with Alx1, but insertion of Domain 2 conferred robust skeletogenic function on Alx4. We used cross-species expression experiments to show that Alx1 proteins from distantly related echinoderms are not interchangeable, although the sequence and function of Domain 2 are highly conserved. We also found that Domain 2 is subject to alternative splicing and provide evidence that this domain was originally gained through exon extension. Our findings show that a gene duplication event permitted the functional specialization of a transcription factor through changes in exon-intron organization and thereby supported the evolution of a major morphological novelty.

Data availability

The following previously published data sets were used

1. Cameron RA
2. Samanta M
3. Yuan A
4. He D
5. Davidson E.
(2009) SpBase:the sea urchin genome database and web site
Publicly available at spBase.org.

http://www.spbase.org/
(2017) Echinobase: an expanding resource for echinoderm genomic information
Publicly available at echinobase.org.

http://www.echinobase.org/
(2015) Hemichordate genomes and deuterostome origins
Publicly available at marinegenomics.oist.jp.

http://marinegenomics.oist.jp/

Article and author information

Author details

Jian Ming Khor

Department of Biological Sciences, Carnegie Mellon University, Pittsburgh, United States

Competing interests
The authors declare that no competing interests exist.

"This ORCID iD identifies the author of this article:" 0000-0002-1428-6770
Charles A Ettensohn

Department of Biological Sciences, Carnegie Mellon University, Pittsburgh, United States

For correspondence
ettensohn@cmu.edu

Competing interests
The authors declare that no competing interests exist.

"This ORCID iD identifies the author of this article:" 0000-0002-3625-0955

Funding

National Science Foundation (IOS-1354973)

Charles A Ettensohn

The funders had no role in study design, data collection and interpretation, or the decision to submit the work for publication.

Copyright

This article is distributed under the terms of the Creative Commons Attribution License permitting unrestricted use and redistribution provided that the original author and source are credited.