The Arabidopsis ALF 4 protein is a regulator of SCF E3 ligases

Abstract

The cullin-RING E3 ligases (CRLs) regulate diverse cellular processes in all eukaryotes. CRL activity is controlled by several proteins or protein complexes, including NEDD8, CAND1, and the CSN Recently, a mammalian protein called Glomulin (GLMN) was shown to inhibit CRLs by binding to the RING BOX (RBX1) subunit and preventing binding to the ubiquitin-conjugating enzyme. Here, we show that ABERRANT LATERAL ROOT FORMATION4 (ALF4) is an ortholog of GLMN The mutant exhibits a phenotype that suggests defects in plant hormone response. We show that ALF4 binds to RBX1 and inhibits the activity of SCF, an E3 ligase responsible for degradation of the Aux/IAA transcriptional repressors. , the mutation destabilizes the CUL1 subunit of the SCF Reduced CUL1 levels are associated with increased levels of the Aux/IAA proteins as well as the DELLA repressors, substrate of SCF We propose that the phenotype is partly due to increased levels of the Aux/IAA and DELLA proteins.

Reprogramming of Cell Fate During Root Regeneration by Transcriptional and Epigenetic Networks

“…Lossof-function mutants of ERF109 or the JA receptor COI1 (CORONATINE INSENSITIVE1) display defective rooting from leaf explants (Zhang et al, 2019). ERF109 upregulates directly ANTHRANILATE SYNTHASEα1 (ASA1) -a ratelimiting enzyme in tryptophan (Trp) biosynthesis -and YUC2 (Bagchi et al, 2018); LFM fail to produce LRs, callus and DNRR (Celenza et al, 1995;Sugimoto et al, 2010; (Fukaki et al, 2002); less callus and DNRR (Shang et al, 2016;Bustillo-Avendaño et al, 2018); PR has less root hairs, Exp in RAM of PR and LRP (Fukaki et al, 2002;Vanneste et al, 2005)…”

“…Then, the degradation of the Aux/IAAs breaks the physical inhibition of the AUXIN RESPONSE FACTORs (ARFs), which bind as transcriptional activators to auxin response elements (AuxREs) in the promoters of auxin response genes (reviewed in more detail in Weijers and Wagner, 2016). In aberrant lateral root formation4-1 (alf4-1) mutants, the CULLIN1 subunit of the SCF TIR1 auxin receptor complex is destabilized leading to increases in the levels of Aux/IAA proteins, the repressors of ARFs (Bagchi et al, 2018). As the name implies, alf4-1 mutant plants are impaired in lateral root formation (Celenza et al, 1995) but they also fail to regenerate roots from leaf explants (Liu et al, 2014).…”

The dynamic nature and regulation of the root clock

“…For example, in the knockout mutant of ABERRANT LATERAL ROOT FORMATION 4 (ALF4), patches of pericycle cells expressing DR5:GFP are specified as founder cells, but do not develop as LRPs due to a defect in cell cycle progression (DiDonato et al, 2004;Dubrovsky et al, 2008). This is might be attributed to the inhibition of auxin signaling, as the SCF TIR1 substrate IAA7 is stabilized in alf4 mutants (Bagchi et al, 2018). Two auxin responsive genes, MEMBRANE ASSOCIATED KINASE REGULATOR 4 (MAKR4) and LATERAL ORGAN BOUNDARIES-DOMAIN 16/ASYMMETRIC LEAVES2-LIKE 18 (LBD16/ASL18), are also known to mediate the transition of the founder cell into a LRP (Goh et al, 2012;Xuan et al, 2015).…”

Regulation of SCFTIR1/AFBs E3 ligase assembly by S-nitrosylation of Arabidopsis SKP1-like1 impacts on auxin signaling

“…Several FBPs show a tissue-specific preference interaction with particular ASKs and more than two hundred FBPs do not interact with any of 19 different assayed ASK proteins, implying that additional regulations for their in vivo interactions within the SCF complex could be necessary [39] . The role of SCF TIR1/AFBs complex during auxin signaling activation has been extensively studied and several proteins including the COP9 signalosome (CSN) complex, RUB/NEDD8, CAND1 and ALF4 have been associated to the exchange of substrate adapters and the regulation of SCF TIR1/AFBs activity [16] , [18] , [3] , [60] , [64] , [89] . In addition, HSP90 and the co-chaperone SGT1 have been related to the stabilization of TIR1 [85] , which may also involve an autocatalytic mechanism [97] .…”