Open AccessMulti-level analysis of the interactions between REVOLUTA and MORE AXILLARY BRANCHES 2 in controlling plant development reveals parallel, independent and antagonistic functions
Author(s) -
SukYoon Hong,
Esther Botterweg-Paredes,
Jasmin Doll,
Tenai Eguen,
Anko Blaakmeer,
Sanne E.A. Matton,
Yakun Xie,
Bjørg Skjøth Lunding,
Ulrike Zentgraf,
Chunmei Guan,
Yuling Jiao,
Stephan Wenkel
Publication year - 2020
Publication title -
development
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.15
H-Index - 36
eISSN - 1477-9129
pISSN - 0950-1991
DOI - 10.1242/dev.183681
Subject(s) - biology , transcription factor , mutant , leucine zipper , microbiology and biotechnology , phenotype , axillary bud , context (archaeology) , transcription (linguistics) , auxin , gene , arabidopsis , genetics , in vitro , explant culture , paleontology , linguistics , philosophy
Class III homeodomain leucine zipper (HD-ZIPIII) transcription factors play fundamental roles in controlling plant development. The known HD-ZIPIII target genes encode proteins involved in the production and dissipation of the auxin signal, HD-ZIPII transcription factors and components that feedback to regulate HD-ZIPIII expression or protein activity. Here, we have investigated the regulatory hierarchies of the control of MORE AXILLARY BRANCHES2 ( MAX2 ) by the HD-ZIPIII protein REVOLUTA (REV). We found that REV can interact with the promoter of MAX2 In agreement, rev10D gain-of-function mutants had increased levels of MAX2 expression, while rev loss-of-function mutants showed lower levels of MAX2 in some tissues. Like REV, MAX2 plays known roles in the control of plant architecture, photobiology and senescence, which prompted us to initiate a multi-level analysis of growth phenotypes of hd-zipIII , max2 and respective higher order mutants thereof. Our data suggest a complex relationship of synergistic and antagonistic activities between REV and MAX2; these interactions appear to depend on the developmental context and do not all involve the direct regulation of MAX2 by REV.