Auxin Binding Protein 1: A Red Herring After All?

Abstract

The natural auxin indole-3-acetic acid is the first hormone identified in plants, and since it plays such a central role in plant growth and development, auxin has been the subject of intensive studies. A central question has been how the auxin signal is perceived by plant cells. The earliest experiments showed the presence of auxin binding particles at the plasma membrane (PM) and in the endoplasmic reticulum (ER) (Hertel et al., 1972). Screens for PM-localized auxin binding activities have led to the photo-affinity labeling and purification of Auxin Binding Protein 1 (ABP1) from maize coleoptile cells (Lö bler and Klä mbt, 1985). Despite observations in different laboratories that ABP1 localized to the PM where it seemed to mediate rapid electrophysiological and cell physiological responses to auxin, the auxin community remained skeptical about the role of ABP1 as auxin receptor for a long time, in part because of its predominant localization in the ER (reviewed by Napier et al., 2002). At some point, ABP1 was even jokingly referred to as a potential red herring in the search for the auxin receptor (Venis, 1995). However, after the first Arabidopsis abp1-1 loss-of-function allele pointed to a key role for ABP1 in cell elongation and division, the auxin community has adopted this abundantly expressed 22-kDa protein as extracellular auxin receptor (reviewed by Napier et al., 2002). Especially in recent years, the role of ABP1 in development has become more firmly established, in part as modulator of clathrinmediated endocytosis and microtubule orientation through its action on the Rho of Plants (ROP) family of GTPases (Robert et al., 2010;Chen et al., 2012Chen et al., , 2014 but also as regulator of auxin-responsive gene expression (Tromas et al., 2013). Recent evidence that auxin-bound ABP1 docks on the extracellular domain of the TRANSMEMBRANE KINASE1 (TMK1) finally linked its apoplastic localization to signaling by the PMassociated ROPs. TMK1 belongs to a small subfamily of four leucine-rich-repeat receptor-like kinases and the quadruple tmk1234 loss-of-function mutant shows several auxin-related phenotypes (Dai et al., 2013;Xu et al., 2014). In addition, auxin-mediated activation of ROP2 and ROP6 and the downstream effects on the actin and microtubule cytoskeleton, respectively, are largely abolished in this mutant (Xu et al., 2014;Grones and Friml, 2015).

An Effective Strategy for Reliably Isolating Heritable and Cas9-Free Arabidopsis Mutants Generated by CRISPR/Cas9-Mediated Genome Editing

“…optimal because of the potential production of truncated proteins Dai et al, 2015;Habets and Offringa, 2015;Pan et al, 2015). Here, we designed two new gRNAs to target two discrete sites in the ABP1 gene ( Fig.…”

Embryonic lethality of Arabidopsis abp1-1 is caused by deletion of the adjacent BSM gene

“…Because of these contradictory reports and the lack of developmental defects in our abp1 null mutants, we and others 15 hypothesized that the embryo lethal phenotype in abp1-1 might not be caused by the disruption of ABP1 . Habets & Offringa 15 went further to suggest that the embryo lethal phenotype might be caused by disrupting the neighbouring gene, At4g02990 ( BSM ).…”

“…On the other hand, our new abp1 alleles, which were null alleles based on well-accepted criteria, lacked obvious developmental defects 12 . Recently, it was suggested that ABP1-related genetic materials be exchanged and re-analysed independently by different laboratories 13–15 . The recent publication of the whole genome sequence of abp1-5 is one step forward in efforts to clarify the ABP1 field 16 .…”

“…Habets & Offringa 15 went further to suggest that the embryo lethal phenotype might be caused by disrupting the neighbouring gene, At4g02990 ( BSM ). Our re-analysis of the Southern blot results using ABP1 as probes suggests that the transfer DNA (T-DNA) insertion in abp1-1 is likely to be complex 4 .…”

Auxin perception and downstream events

“…Since the discovery of ABP1 in 1972, research into this proposed auxin receptor has been surrounded with controversy [7–9]. ABP1 is a 22 kDa protein with a C-terminal KDEL ER-retention signal [10,11]; over 90% of ABP1 is ER-localized [12].…”