Arabidopsis HT1 kinase controls stomatal movements in response to CO2
Guard cells, which form stomata in leaf epidermes, sense a multitude of environmental signals and integrate this information to regulate stomatal movements 1 , 2 . Compared with the advanced understanding of light and water stress responses in guard cells 2 , 3 , 4 , the molecular mechanisms that un...
Gespeichert in:
Veröffentlicht in: | Nature cell biology 2006-04, Vol.8 (4), p.391-397 |
---|---|
Hauptverfasser: | , , , , , |
Format: | Artikel |
Sprache: | eng |
Schlagworte: | |
Online-Zugang: | Volltext |
Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
Zusammenfassung: | Guard cells, which form stomata in leaf epidermes, sense a multitude of environmental signals and integrate this information to regulate stomatal movements
1
,
2
. Compared with the advanced understanding of light and water stress responses in guard cells
2
,
3
,
4
, the molecular mechanisms that underlie stomatal CO
2
signalling have remained relatively obscure. With a high-throughput leaf thermal imaging CO
2
screen, we report the isolation of two allelic
Arabidopsis
mutants (
high leaf temperature 1
;
ht1-1
and
ht1-2
) that are altered in their ability to control stomatal movements in response to CO
2
. The strong allele,
ht1-2
, exhibits a markedly impaired CO
2
response but shows functional responses to blue light, fusicoccin and abscisic acid (ABA), indicating a role for
HT1
in stomatal CO
2
signalling.
HT1
encodes a protein kinase that is expressed mainly in guard cells. Phosphorylation assays demonstrate that the activity of the HT1 protein carrying the
ht1-1
or
ht1-2
mutation is greatly impaired or abolished, respectively. Furthermore, dominant-negative HT1(K113W) transgenic plants, which lack HT1 kinase activity, show a disrupted CO
2
response. These findings indicate that the HT1 kinase is important for regulation of stomatal movements and its function is more pronounced in response to CO
2
than it is to ABA or light. |
---|---|
ISSN: | 1465-7392 1476-4679 |
DOI: | 10.1038/ncb1387 |