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Timing is everything: highly specific and transient expression of a MAP kinase determines auxin-induced leaf venation patterns in Arabidopsis.

Stanko V, Giuliani C, Retzer K, Djamei A, Wahl V, Wurzinger B, Wilson C, Heberle-Bors E, Teige M, Kragler F - Mol Plant (2014)

Bottom Line: Moreover, cotyledons of mpk10 and mkk2 mutants have reduced vein complexity, which can be reversed by inhibiting polar auxin transport (PAT).Auxin does not affect AtMPK10 expression while treatment with the PAT inhibitor HFCA extends the expression in leaves and reverses the mpk10 mutant phenotype.These results suggest that the AtMKK2-AtMPK10 MAPK module regulates venation complexity by altering PAT efficiency.

View Article: PubMed Central - PubMed

Affiliation: Department of Plant Molecular Biology, Max. F. Perutz Laboratories, University of Vienna, Dr. Bohrgasse 9/4, Vienna, A-1030, Austria Present address: Felix-Klein-Gymnasium, Böttingerstraße 17, D-37073 Göttingen, Germany.

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Putative Model for the Function of the AtMKK2/AtMPK10 Kinase Cascade on PAT and Vascular Development.(A) MKK2 and MPK10 affect directly or indirectly the vesicle trafficking efficiency within the vascular precursor cells. This affects also the transport of the auxin carrier to the cell membrane thereby altering the polar auxin transport and vascular development (for detailed explanation, see the ‘Discussion’ section).(B) The effect of MKK2/MPK10 on leaf vascular development in the context of auxin channeling. The model integrates known effects of PAT inhibitors on wild-type leaves, AtMPK10 and DR5 expression patterns (= auxin maxima), atmpk10 and atmkk2 mutant phenotypes, AtMPK10 overexpression, and treatment of the mutants with the PAT inhibitor HFCA. Here the MKK2/MPK10 kinase cascade controls number and ‘strength’ of auxin maxima (red) as starting sites for provascular strands formation. In mpk10 and mkk2 mutant plants, auxin maxima are fewer and in smaller areas leading to a less complex vasculature. Thus, plants lacking MPK10 or MKK2 activity are less sensitive to PAT inhibitors and form a vasculature exhibiting a similar complexity to the wild-type.
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Figure 6: Putative Model for the Function of the AtMKK2/AtMPK10 Kinase Cascade on PAT and Vascular Development.(A) MKK2 and MPK10 affect directly or indirectly the vesicle trafficking efficiency within the vascular precursor cells. This affects also the transport of the auxin carrier to the cell membrane thereby altering the polar auxin transport and vascular development (for detailed explanation, see the ‘Discussion’ section).(B) The effect of MKK2/MPK10 on leaf vascular development in the context of auxin channeling. The model integrates known effects of PAT inhibitors on wild-type leaves, AtMPK10 and DR5 expression patterns (= auxin maxima), atmpk10 and atmkk2 mutant phenotypes, AtMPK10 overexpression, and treatment of the mutants with the PAT inhibitor HFCA. Here the MKK2/MPK10 kinase cascade controls number and ‘strength’ of auxin maxima (red) as starting sites for provascular strands formation. In mpk10 and mkk2 mutant plants, auxin maxima are fewer and in smaller areas leading to a less complex vasculature. Thus, plants lacking MPK10 or MKK2 activity are less sensitive to PAT inhibitors and form a vasculature exhibiting a similar complexity to the wild-type.

Mentions: These results pointed to a possible role of the AtMKK2/AtMPK10 kinase cascade in PAT controlling vascular development (Figure 6). As treatment of the mpk10 mutant with PAT inhibitors had the same effect as expression of AtMPK10 or AtMKK2 in this mutant background, it seems that the AtMKK2/AtMPK10 module plays a role in the action of PAT inhibitors. PAT inhibitors such as HFCA, NPA, or TIBA are synthetic substances but it is widely accepted that they mimic the action of natural PAT inhibitors (Murphy et al., 2000).


Timing is everything: highly specific and transient expression of a MAP kinase determines auxin-induced leaf venation patterns in Arabidopsis.

Stanko V, Giuliani C, Retzer K, Djamei A, Wahl V, Wurzinger B, Wilson C, Heberle-Bors E, Teige M, Kragler F - Mol Plant (2014)

Putative Model for the Function of the AtMKK2/AtMPK10 Kinase Cascade on PAT and Vascular Development.(A) MKK2 and MPK10 affect directly or indirectly the vesicle trafficking efficiency within the vascular precursor cells. This affects also the transport of the auxin carrier to the cell membrane thereby altering the polar auxin transport and vascular development (for detailed explanation, see the ‘Discussion’ section).(B) The effect of MKK2/MPK10 on leaf vascular development in the context of auxin channeling. The model integrates known effects of PAT inhibitors on wild-type leaves, AtMPK10 and DR5 expression patterns (= auxin maxima), atmpk10 and atmkk2 mutant phenotypes, AtMPK10 overexpression, and treatment of the mutants with the PAT inhibitor HFCA. Here the MKK2/MPK10 kinase cascade controls number and ‘strength’ of auxin maxima (red) as starting sites for provascular strands formation. In mpk10 and mkk2 mutant plants, auxin maxima are fewer and in smaller areas leading to a less complex vasculature. Thus, plants lacking MPK10 or MKK2 activity are less sensitive to PAT inhibitors and form a vasculature exhibiting a similar complexity to the wild-type.
© Copyright Policy - creative-commons
Related In: Results  -  Collection

License 1 - License 2
Show All Figures
getmorefigures.php?uid=PMC4228985&req=5

Figure 6: Putative Model for the Function of the AtMKK2/AtMPK10 Kinase Cascade on PAT and Vascular Development.(A) MKK2 and MPK10 affect directly or indirectly the vesicle trafficking efficiency within the vascular precursor cells. This affects also the transport of the auxin carrier to the cell membrane thereby altering the polar auxin transport and vascular development (for detailed explanation, see the ‘Discussion’ section).(B) The effect of MKK2/MPK10 on leaf vascular development in the context of auxin channeling. The model integrates known effects of PAT inhibitors on wild-type leaves, AtMPK10 and DR5 expression patterns (= auxin maxima), atmpk10 and atmkk2 mutant phenotypes, AtMPK10 overexpression, and treatment of the mutants with the PAT inhibitor HFCA. Here the MKK2/MPK10 kinase cascade controls number and ‘strength’ of auxin maxima (red) as starting sites for provascular strands formation. In mpk10 and mkk2 mutant plants, auxin maxima are fewer and in smaller areas leading to a less complex vasculature. Thus, plants lacking MPK10 or MKK2 activity are less sensitive to PAT inhibitors and form a vasculature exhibiting a similar complexity to the wild-type.
Mentions: These results pointed to a possible role of the AtMKK2/AtMPK10 kinase cascade in PAT controlling vascular development (Figure 6). As treatment of the mpk10 mutant with PAT inhibitors had the same effect as expression of AtMPK10 or AtMKK2 in this mutant background, it seems that the AtMKK2/AtMPK10 module plays a role in the action of PAT inhibitors. PAT inhibitors such as HFCA, NPA, or TIBA are synthetic substances but it is widely accepted that they mimic the action of natural PAT inhibitors (Murphy et al., 2000).

Bottom Line: Moreover, cotyledons of mpk10 and mkk2 mutants have reduced vein complexity, which can be reversed by inhibiting polar auxin transport (PAT).Auxin does not affect AtMPK10 expression while treatment with the PAT inhibitor HFCA extends the expression in leaves and reverses the mpk10 mutant phenotype.These results suggest that the AtMKK2-AtMPK10 MAPK module regulates venation complexity by altering PAT efficiency.

View Article: PubMed Central - PubMed

Affiliation: Department of Plant Molecular Biology, Max. F. Perutz Laboratories, University of Vienna, Dr. Bohrgasse 9/4, Vienna, A-1030, Austria Present address: Felix-Klein-Gymnasium, Böttingerstraße 17, D-37073 Göttingen, Germany.

Show MeSH
Related in: MedlinePlus