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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.

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