A major isoform of the maize plasma membrane H(+)-ATPase: characterization and induction by auxin in coleoptiles
| Autor: | Ignacio Frias, Maria T. Caldeira, José R. Pérez-Castiñeira, Francisco A. Culiáñez-Macià, Achim Hager, Harald Stransky, Montserrat Pages, Ramón Serrano, Oliver Kuppinger, Juan P. Navarro-Avino |
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| Rok vydání: | 1996 |
| Předmět: |
Gene isoform
DNA Plant ATPase Molecular Sequence Data In situ hybridization Plant Science Biology Genes Plant Zea mays Auxin Guard cell Tissue Distribution Amino Acid Sequence RNA Messenger Cloning Molecular chemistry.chemical_classification Base Sequence Indoleacetic Acids fungi Cell Membrane food and beverages Cell Biology Blot Isoenzymes Proton-Translocating ATPases Coleoptile chemistry Biochemistry Enzyme Induction biology.protein Phloem Research Article |
| Zdroj: | The Plant cell. 8(9) |
| ISSN: | 1040-4651 |
| Popis: | The plasma membrane (PM) H(+)-ATPase has been proposed to play important transport and regulatory roles in plant physiology, including its participation in auxin-induced acidification in coleoptile segments. This enzyme is encoded by a family of genes differing in tissue distribution, regulation, and expression level. A major expressed isoform of the maize PM H(+)-ATPase (MHA2) has been characterized. RNA gel blot analysis indicated that MHA2 is expressed in all maize organs, with highest levels being in the roots. In situ hybridization of sections from maize seedlings indicated enriched expression of MHA2 in stomatal guard cells, phloem cells, and root epidermal cells. MHA2 mRNA was induced threefold when nonvascular parts of the coleoptile segments were treated with auxin. This induction correlates with auxin-triggered proton extrusion by the same part of the segments. The PM H(+)-ATPase in the vascular bundies does not contribute significantly to auxin-induced acidification, is not regulated by auxin, and masks the auxin effect in extracts of whole coleoptile segments. We conclude that auxin-induced acidification in coleoptile segments most often occurs in the nonvascular tissue and is mediated, at least in part, by increased levels of MHA2. |
| Databáze: | OpenAIRE |
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