Embryo - lethal phenotypes in early mutants are due to abp 1 disruption of the neighboring gene BSM

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 T-DNA Arabidopsis insertional knock-out alleles ( and ) and the wild type-like abp1-1 abp1-1s phenotypes of other recently described loss-of-function alleles ( and abp1-c1 ) questions the biological importance of ABP1 and relevance of the abp1-TD1 previous genetic studies. Here we show that there is no hidden copy of the gene in the genome but the embryo-lethal phenotypes of ABP1 Arabidopsis and alleles are very similar to the knock-out phenotypes of the abp1-1 abp1-1s neighboring gene, ( ). Furthermore, the allelic BELAYA SMERT BSM complementation test between and alleles shows that the bsm abp1 embryo-lethality in the and alleles is caused by the off-target abp1-1 abp1-1s disruption of the locus by the T-DNA insertions. This clarifies the BSM controversy of different phenotypes among published knock-out alleles abp1 and asks for reflections on the developmental role of ABP1. Jiří Friml ( ) Corresponding author: [email protected] Michalko J, Dravecká M, Bollenbach T and Friml J. How to cite this article: Embryo-lethal phenotypes in early mutants are due to abp1 2015, :1104 (doi: disruption of the neighboring gene [version 1; referees: 3 approved] BSM F1000Research 4 ) 10.12688/f1000research.7143.1 © 2015 Michalko J . This is an open access article distributed under the terms of the , which Copyright: et al Creative Commons Attribution Licence permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Data associated with the article are available under the terms of the (CC0 1.0 Public domain dedication). Creative Commons Zero "No rights reserved" data waiver This work was supported by ERC Independent Research grant (ERC-2011-StG-20101109-PSDP to JF). JM internship was Grant information: supported by the grant “Action Austria – Slovakia”. Competing interests: No competing interests were disclosed. 23 Oct 2015, :1104 (doi: ) First published: 4 10.12688/f1000research.7143.1 1,2 1 1