Embryo-lethal phenotypes in early abp1 mutants are due to disruption of the neighboring BSM gene Journal Article


Author(s): Michalko, Jaroslav; Dravecká, Marta; Bollenbach, Tobias; Friml, Jiří
Article Title: Embryo-lethal phenotypes in early abp1 mutants are due to disruption of the neighboring BSM gene
Affiliation IST Austria
Abstract: The Auxin Binding Protein1 (ABP1) has been identified based on its ability to bind auxin with high affinity and studied for a long time as a prime candidate for the extracellular auxin receptor responsible for mediating in particular the fast non-transcriptional auxin responses. However, the contradiction between the embryo-lethal phenotypes of the originally described Arabidopsis T-DNA insertional knock-out alleles (abp1-1 and abp1-1s) and the wild type-like phenotypes of other recently described loss-of-function alleles (abp1-c1 and abp1-TD1) questions the biological importance of ABP1 and relevance of the previous genetic studies. Here we show that there is no hidden copy of the ABP1 gene in the Arabidopsis genome but the embryo-lethal phenotypes of abp1-1 and abp1-1s alleles are very similar to the knock-out phenotypes of the neighboring gene, BELAYA SMERT (BSM). Furthermore, the allelic complementation test between bsm and abp1 alleles shows that the embryo-lethality in the abp1-1 and abp1-1s alleles is caused by the off-target disruption of the BSM locus by the T-DNA insertions. This clarifies the controversy of different phenotypes among published abp1 knock-out alleles and asks for reflections on the developmental role of ABP1.
Journal Title: F1000 Research
Volume: 4
ISSN: 2046-1402
Publisher: F1000 Research Ltd.  
Date Published: 2015-10-01
Start Page: Article number: 1104
Copyright Statement: CC-BY
Sponsor: This work was supported by ERC Independent Research grant (ERC-2011-StG-20101109-PSDP to JF). JM internship was supported by the grant “Action Austria – Slovakia”.
URL:
DOI: 10.12688/f1000research.7143.1
Notes: Data associated with the article are available under the terms of the Creative Commons Zero "No rights reserved" data waiver (CC0 1.0 Public domain dedication). Data availability: F1000Research: Dataset 1. Dataset 1, 10.5256/f1000research.7143.d104552 F1000Research: Dataset 2. Dataset 2, 10.5256/f1000research.7143.d104553 F1000Research: Dataset 3. Dataset 3, 10.5256/f1000research.7143.d104554
Open access: yes (OA journal)