Consequences of a Deficit in Vitamin B6 Biosynthesis de Novo for Hormone Homeostasis and Root Development in Arabidopsis

Autor: Svetlana Boycheva, Jakub Rolcik, Teresa B. Fitzpatrick, Thomas Boller, Ana Dominguez
Rok vydání: 2014
Předmět:
0106 biological sciences
endocrine system
endocrine system diseases
Physiology
Mutant
Plant Science
digestive system
01 natural sciences
03 medical and health sciences
chemistry.chemical_compound
Arabidopsis Proteins/metabolism/physiology
Auxin
Arabidopsis
Genetics
medicine
Nitrogenous Group Transferases/metabolism/physiology
Arabidopsis thaliana
Gene
Pyridoxal
030304 developmental biology
Plant Roots/growth & development
2. Zero hunger
chemistry.chemical_classification
0303 health sciences
biology
Indoleacetic Acids/metabolism
Homeostasis/physiology
Meristem
Pyridoxine
biology.organism_classification
ddc:580
Arabidopsis/growth & development/metabolism/physiology
Phenotype
chemistry
Biochemistry
Vitamin B 6/biosynthesis/physiology
Plant Growth Regulators/metabolism/physiology
010606 plant biology & botany
medicine.drug
Zdroj: Plant physiology
Plant Physiology, Vol. 167, No 1 (2015) pp. 102-117
ISSN: 1532-2548
0032-0889
DOI: 10.1104/pp.114.247767
Popis: Vitamin B6 (pyridoxal 5′-phosphate) is an essential cofactor of many metabolic enzymes. Plants biosynthesize the vitamin de novo employing two enzymes, pyridoxine synthase1 (PDX1) and PDX2. In Arabidopsis (Arabidopsis thaliana), there are two catalytically active paralogs of PDX1 (PDX1.1 and PDX1.3) producing the vitamin at comparable rates. Since single mutants are viable but the pdx1.1 pdx1.3 double mutant is lethal, the corresponding enzymes seem redundant. However, the single mutants exhibit substantial phenotypic differences, particularly at the level of root development, with pdx1.3 being more impaired than pdx1.1. Here, we investigate the differential regulation of PDX1.1 and PDX1.3 by identifying factors involved in their disparate phenotypes. Swapped-promoter experiments clarify the presence of distinct regulatory elements in the upstream regions of both genes. Exogenous sucrose (Suc) triggers impaired ethylene production in both mutants but is more severe in pdx1.3 than in pdx1.1. Interestingly, Suc specifically represses PDX1.1 expression, accounting for the stronger vitamin B6 deficit in pdx1.3 compared with pdx1.1. Surprisingly, Suc enhances auxin levels in pdx1.1, whereas the levels are diminished in pdx1.3. In the case of pdx1.3, the previously reported reduced meristem activity combined with the impaired ethylene and auxin levels manifest the specific root developmental defects. Moreover, it is the deficit in ethylene production and/or signaling that triggers this outcome. On the other hand, we hypothesize that it is the increased auxin content of pdx1.1 that is responsible for the root developmental defects observed therein. We conclude that PDX1.1 and PDX1.3 play partially nonredundant roles and are differentially regulated as manifested in disparate root growth impairment morphologies.
Databáze: OpenAIRE