Auxin triggers a genetic switch
The plant hormone auxin promotes the degradation of inhibitors of ARF transcription factors to control plant development, but the role of auxin in patterning has been unclear. The ARF protein MONOPTEROS is shown to induce both its own expression and that of its inhibitor, with auxin acting as a thre...
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Veröffentlicht in: | Nature cell biology 2011-05, Vol.13 (5), p.611-615 |
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Sprache: | eng |
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Zusammenfassung: | The plant hormone auxin promotes the degradation of inhibitors of ARF transcription factors to control plant development, but the role of auxin in patterning has been unclear. The ARF protein MONOPTEROS is shown to induce both its own expression and that of its inhibitor, with auxin acting as a threshold-specific trigger to switch this feedback system to MONOPTEROS accumulation.
Cell specification in development requires robust gene-regulatory responses to transient signals. In plants, the small signalling molecule auxin has been implicated in diverse developmental processes
1
,
2
. Auxin promotes the degradation of AUXIN/INDOLE-3-ACETIC ACID (AUX/IAA) inhibitors that prevent AUXIN RESPONSE FACTOR (ARF) transcription factors from regulating their target genes
1
,
3
. However, the precise role of auxin in patterning has remained unclear, the view of auxin acting as a morphogen is controversial
4
,
5
and the transcriptional control of the
ARF
genes themselves is barely explored
6
. Here, we demonstrate by experimental and computational analyses that the
Arabidopsis
ARF protein MONOPTEROS (MP) controls its own expression and the expression of its AUX/IAA inhibitor BODENLOS (BDL), with auxin acting as a threshold-specific trigger by promoting the degradation of the inhibitor. Our results suggest a general mechanism for how the transient accumulation of auxin activates self-sustaining or hysteretic feedback systems of interacting auxin-response proteins that, similarly to other genetic switches, result in unequivocal developmental responses. |
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ISSN: | 1465-7392 1476-4679 |
DOI: | 10.1038/ncb2212 |