Mitogen-activated protein kinase 6 integrates phosphate and iron responses for indeterminate root growth in Arabidopsis thaliana

Abscission is a developmental program that results in the active shedding of infected or nonfunctional organs from a plant body. Here, we establish a signaling pathway that controls abscission in Arabidopsis thaliana from ligand, to receptors, to downstream effectors. Loss of function mutations in Inflorescence Deficient in Abscission (IDA), which encodes a predicted secreted small protein, the receptor-like protein kinases HAESA (HAE) and HAESA-like 2 (HSL2), the Mitogen-Activated Protein Kinase Kinase 4 (MKK4) and MKK5, and a dominant-negative form of Mitogen-Activated Protein Kinase 6 (MPK6) in a mpk3 mutant background all have abscission-defective phenotypes. Conversely, expression of constitutively active MKKs rescues the abscission-defective phenotype of hae hsl2 and ida plants. Additionally, in hae hsl2 and ida plants, MAP kinase activity is reduced in the receptacle, the part of the stem that holds the floral organs. Plants overexpressing IDA in a hae hsl2 background have abscission defects, indicating HAE and HSL2 are epistatic to IDA. Taken together, these results suggest that the sequential action of IDA, HAE and HSL2, and a MAP kinase cascade regulates the programmed separation of cells in the abscission zone.

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Mitogen-activated protein kinase 4 is involved in the regulation of mitotic and cytokinetic microtubule transitions in Arabidopsis thaliana

New Phytologist ◽

10.1111/j.1469-8137.2010.03565.x ◽

2010 ◽

Vol 189 (4) ◽

pp. 1069-1083 ◽

Cited By ~ 77

Author(s):

Martina Beck ◽

George Komis ◽

Anja Ziemann ◽

Diedrik Menzel ◽

Jozef Šamaj

Keyword(s):

Arabidopsis Thaliana ◽

Protein Kinase ◽

Mitogen Activated Protein Kinase ◽

Mitogen Activated Protein

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Mitogen-Activated Protein Kinase 6 and Ethylene and Auxin Signaling Pathways Are Involved in Arabidopsis Root-System Architecture Alterations by Trichoderma atroviride

Molecular Plant-Microbe Interactions ◽

10.1094/mpmi-01-15-0005-r ◽

2015 ◽

Vol 28 (6) ◽

pp. 701-710 ◽

Cited By ~ 52

Author(s):

Hexon Angel Contreras-Cornejo ◽

Jesús Salvador López-Bucio ◽

Alejandro Méndez-Bravo ◽

Lourdes Macías-Rodríguez ◽

Maricela Ramos-Vega ◽

...

Keyword(s):

Protein Kinase ◽

Root Growth ◽

System Architecture ◽

Primary Root ◽

Root System Architecture ◽

Mitogen Activated Protein Kinase ◽

Auxin Signaling ◽

Trichoderma Atroviride ◽

Mitogen Activated Protein ◽

Primary Root Growth

Trichoderma atroviride is a symbiotic fungus that interacts with roots and stimulates plant growth and defense. Here, we show that Arabidopsis seedlings cocultivated with T. atroviride have an altered root architecture and greater biomass compared with axenically grown seedlings. These effects correlate with increased activity of mitogen-activated protein kinase 6 (MPK6). The primary roots of mpk6 mutants showed an enhanced growth inhibition by T. atroviride when compared with wild-type (WT) plants, while T. atroviride increases MPK6 activity in WT roots. It was also found that T. atroviride produces ethylene (ET), which increases with l-methionine supply to the fungal growth medium. Analysis of growth and development of WT seedlings and etr1, ein2, and ein3 ET-related Arabidopsis mutants indicates a role for ET in root responses to the fungus, since etr1 and ein2 mutants show defective root-hair induction and enhanced primary-root growth inhibition when cocultivated with T. atroviride. Increased MPK6 activity was evidenced in roots of ctr1 mutants, which correlated with repression of primary root growth, thus connecting MPK6 signaling with an ET response pathway. Auxin-inducible gene expression analysis using the DR5:uidA reporter construct further revealed that ET affects auxin signaling through the central regulator CTR1 and that fungal-derived compounds, such as indole-3-acetic acid and indole-3-acetaldehyde, induce MPK6 activity. Our results suggest that T. atroviride likely alters root-system architecture modulating MPK6 activity and ET and auxin action.

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