Timing Is Everything： Highly Specific and Transient Expression of a MAP Kinase Determines Auxin-Induced Leaf Venation Patterns in Arabidopsis

• Published in: Molecular plant 2014-11, Vol.7 (11), p.1637-1652
• Main Authors: Stanko, Vera, Giuliani, Concetta, Retzer, Katarzyna, Djamei, Armin, Wahl, Vanessa, Wurzinger, Bernhard, Wilson, Cathal, Heberle-Bors, Erwin, Teige, Markus, Kragler, Friedrich
• Format: Article
• Language: English
• Subjects: Arabidopsis - genetics; Arabidopsis - metabolism; Arabidopsis MAP kinase; Arabidopsis Proteins - genetics; Arabidopsis Proteins - metabolism; Enzyme Activation; Gene Expression Regulation, Plant; Indoleacetic Acids - metabolism; leaf development; leaf venation pattern; MAP Kinase Signaling System; MAPK; MAP激酶; Mitogen-Activated Protein Kinase Kinases - genetics; Mitogen-Activated Protein Kinase Kinases - metabolism; Phosphorylation; Plant Leaves - anatomy & histology; polar auxin transport; Signal Transduction; 促分裂原活化蛋白激酶; 叶脉; 图案化; 拟南芥; 生长素; 瞬时表达
• ISSN: 1674-2052; 1752-9867
• DOI: 10.1093/mp/ssu080

Mitogen-activated protein kinase （MAPK） cascades are universal signal transduction modules present in all eukaryotes. In plants, MAPK cascades were shown to regulate cell division, developmental processes, stress responses, and hormone pathways. The subgroup A of Arabidopsis MAPKs consists of AtMPK3, AtMPK6, and AtMPK10. AtMPK3 and AtMPK6 are activated by their upstream MAP kinase kinases （MKKs） AtMKK4 and AtMKK5 in response to biotic and abiotic stress. In addition, they were identified as key regulators of stomatal development and patterning. AtMPKIO has long been considered as a pseudo-gene, derived from a gene duplication of AtMPK6. Here we show that AtMPKIO is expressed highly but very transiently in seedlings and at sites of local auxin maxima leaves. MPK10 encodes a functional kinase and interacts with the upstream MAP kinase kinase （MAPKK） AtMKK2. mpklO mutants are delayed in flowering in long-day conditions and in continuous light. 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 AtMPKIO expression while treatment with the PAT inhibitor HFCA extends the expression in leaves and reverses the mpklO mutant phenotype. These results suggest that the AtMKK2-AtMPK10 MAPK module regulates venation complexity by altering PAT efficiency.