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 |
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Main Authors: | , , , |
Format: | Journal Article |
Language: | English |
Published: |
Switzerland
Frontiers Media S.A
13-11-2018
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Subjects: | |
Online Access: | Get full text |
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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
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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
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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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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 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 |