Light- and IAA-regulated ACC synthase gene (PnACS) from Pharbitis nil and its possible role in IAA-mediated flower inhibition
The light- and indole-3-acetic acid (IAA)-regulated 1-aminocyclopropane-1-carboxylic acid (ACC) synthase gene (PnACS) from Pharbitis nil was isolated. Here, it was shown that the gene was expressed in cotyledons, petioles, hypocotyls, root and shoot apexes both in light- and dark-grown seedlings. Th...
| Veröffentlicht in: | Journal of plant physiology. - 1979. - 166(2009), 2 vom: 30. Jan., Seite 192-202 |
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| 1. Verfasser: | |
| Weitere Verfasser: | , , |
| Format: | Online-Aufsatz |
| Sprache: | English |
| Veröffentlicht: |
2009
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| Zugriff auf das übergeordnete Werk: | Journal of plant physiology |
| Schlagworte: | Journal Article Research Support, Non-U.S. Gov't DNA, Complementary Indoleacetic Acids RNA, Messenger indoleacetic acid 6U1S09C61L Lyases EC 4.- 1-aminocyclopropanecarboxylate synthase |
| Zusammenfassung: | The light- and indole-3-acetic acid (IAA)-regulated 1-aminocyclopropane-1-carboxylic acid (ACC) synthase gene (PnACS) from Pharbitis nil was isolated. Here, it was shown that the gene was expressed in cotyledons, petioles, hypocotyls, root and shoot apexes both in light- and dark-grown seedlings. The highest expression level of PnACS was found in the roots. IAA applied to the cotyledons of P. nil seedlings caused a clear increase of PnACS messenger accumulation in all the organs examined. In this case, the most IAA-responsive were the hypocotyls. Our studies revealed that the PnACS transcript level in the cotyledons exhibited diurnal oscillations under both long-day (LD) and short-day (SD) conditions. IAA applied at the beginning of inductive darkness caused a dramatic increase in the expression of PnACS, suggesting that the inhibitory effect of IAA on P. nil flowering may result from its stimulatory effect on ethylene production |
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| Beschreibung: | Date Completed 10.06.2009 Date Revised 30.09.2020 published: Print-Electronic GENBANK: DQ235256 Citation Status MEDLINE |
| ISSN: | 1618-1328 |
| DOI: | 10.1016/j.jplph.2008.02.013 |