Redundancy, Feedback, and Robustness in the Arabidopsis thaliana BZR/BEH Gene Family

Organismal development is remarkably robust, tolerating stochastic errors to produce consistent, so-called canalized adult phenotypes. The mechanistic underpinnings of developmental robustness are poorly understood, but recent studies implicate certain features of genetic networks such as functional...

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Published in:Frontiers in genetics Vol. 9; p. 523
Main Authors: Lachowiec, Jennifer, Mason, G Alex, Schultz, Karla, Queitsch, Christine
Format: Journal Article
Language:English
Published: Switzerland Frontiers Media S.A 13-11-2018
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Summary:Organismal development is remarkably robust, tolerating stochastic errors to produce consistent, so-called canalized adult phenotypes. The mechanistic underpinnings of developmental robustness are poorly understood, but recent studies implicate certain features of genetic networks such as functional redundancy, connectivity, and feedback. Here, we examine the / gene family, whose function contributes to embryonic stem development in the plant , to test current assumptions on functional redundancy and trait robustness. Our analyses of / gene mutants and mutant combinations revealed that functional redundancy among these gene family members is not necessary for trait robustness. Connectivity is another commonly cited determinant of robustness; however, we found no correlation between connectivity among gene family members or their connectivity with other transcription factors and effects on developmental robustness. Instead, our data suggest that , the earliest diverged family member, modulates developmental robustness. We present evidence indicating that regulatory cross-talk among gene family members is integrated by to promote wild-type levels of developmental robustness. Further, the chaperone HSP90, a known determinant of developmental robustness, appears to act via BEH4 in maintaining robustness of embryonic stem length. In summary, we demonstrate that even among closely related transcription factors, trait robustness can arise through the activity of a single gene family member, challenging common assumptions about the molecular underpinnings of robustness.
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Reviewed by: Tetsu Kinoshita, Yokohama City University, Japan; Neil Youngson, University of New South Wales, Australia
Edited by: Alexander William Shingleton, University of Illinois at Chicago, United States
Present address: Jennifer Lachowiec, Plant Sciences and Plant Pathology, Montana State University, Bozeman, MT, United States; G. Alex Mason, Department of Plant Biology and Genome Center, University of California, Davis, Davis, CA, United States; Karla Schultz, College of Veterinary Medicine, Colorado State University, Fort Collins, CO, United States
This article was submitted to Epigenomics and Epigenetics, a section of the journal Frontiers in Genetics
ISSN:1664-8021
1664-8021
DOI:10.3389/fgene.2018.00523