TY - JOUR
T1 - The ALF4 protein is a regulator of SCF E3 ligases
AU - Bagchi, Rammyani
AU - Melnyk, Charles W
AU - Christ, Gideon
AU - Winkler, Martin
AU - Kirchsteiner, Kerstin
AU - Salehin, Mohammad
AU - Mergner, Julia
AU - Niemeyer, Michael
AU - Schwechheimer, Claus
AU - Calderón Villalobos, Luz Irina A
AU - Estelle, Mark
PY - 2018
Y1 - 2018
N2 - 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.
AB - 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.
M3 - Article
VL - 37
SP - 255
EP - 268
JO - Unknown journal
JF - Unknown journal
IS - 2
ER -