The pea branching RMS2 gene encodes the PsAFB4/5 auxin receptor and is involved in an auxin-strigolactone regulation loop
0301 basic medicine
570
Arabidopsis
Picloram
Receptors, Cell Surface
QH426-470
biosynthèse
03 medical and health sciences
Plant Growth Regulators
Gene Expression Regulation, Plant
Medicago truncatula
Genetics
[SDV.BV]Life Sciences [q-bio]/Vegetal Biology
Pisum sativum
Plant Proteins
580
amélioration génétique
Vegetal Biology
auxine
Indoleacetic Acids
Arabidopsis Proteins
arabidopsis thaliana
pois
Biologie végétale
Plant Shoots
Research Article
Signal Transduction
DOI:
10.1371/journal.pgen.1007089
Publication Date:
2017-12-08T19:28:03Z
AUTHORS (14)
ABSTRACT
Strigolactones (SLs) are well known for their role in repressing shoot branching. In pea, increased transcript levels of SL biosynthesis genes are observed in stems of highly branched SL deficient (ramosus1 (rms1) and rms5) and SL response (rms3 and rms4) mutants indicative of negative feedback control. In contrast, the highly branched rms2 mutant has reduced transcript levels of SL biosynthesis genes. Grafting studies and hormone quantification led to a model where RMS2 mediates a shoot-to-root feedback signal that regulates both SL biosynthesis gene transcript levels and xylem sap levels of cytokinin exported from roots. Here we cloned RMS2 using synteny with Medicago truncatula and demonstrated that it encodes a putative auxin receptor of the AFB4/5 clade. Phenotypes similar to rms2 were found in Arabidopsis afb4/5 mutants, including increased shoot branching, low expression of SL biosynthesis genes and high auxin levels in stems. Moreover, afb4/5 and rms2 display a specific resistance to the herbicide picloram. Yeast-two-hybrid experiments supported the hypothesis that the RMS2 protein functions as an auxin receptor. SL root feeding using hydroponics repressed auxin levels in stems and down-regulated transcript levels of auxin biosynthesis genes within one hour. This auxin down-regulation was also observed in plants treated with the polar auxin transport inhibitor NPA. Together these data suggest a homeostatic feedback loop in which auxin up-regulates SL synthesis in an RMS2-dependent manner and SL down-regulates auxin synthesis in an RMS3 and RMS4- dependent manner.
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