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The mutant ghr1 was isolated in a genetic mutant screening in a low-pH growth
medium. This mutant losses more water and wilts faster than wild-type plants
under drought condition, and ABA- and H 2 O 2 -induced stomatal closure were
impaired in this mutant (Hua et al. 2012 ). Patch clamping experimental results
showed that the mutation of GHR1 impaired H 2 O 2 activation of Ca 2 + channels,
and ABA and H 2 O 2 activation of S-type anion channel currents (Hua et al. 2012 ).
Further analysis showed that GHR1 functions downstream of ABI1, ABI2, OST1,
and H 2 O 2 , but upstream of SLAC1 (Hua et al. 2012 ).
Calcineurin-B-like proteins (CBLs) are calcium sensors, interact with, and
modulate the activity of CBL-interacting protein kinases (CIPKs), which fur-
ther regulate download targets by phosphorylation. Arabidopsis genome has 10
CBLs and 25 CIPKs, and CBL1 and CBL9 were found functioning in guard cells
by interacting with and targeting CIPK23 to the plasma membrane of guard cells
(Cheong et al. 2007 ). The loss-of-function mutant cpk23 showed a reduced tran-
spirational water loss and ABA hypersensitive phenotypes in stomatal opening and
closure (Cheong et al. 2007 ).
AtMRP5, a members of ATP-binding cassette (ABC) family, has been sug-
gested functioning in guard cells as a channel (Gaedeke et al. 2001 ), and the sto-
matal closure in atmrp5 mutant is insensitive to ABA and external Ca 2 + (Klein
et al. 2003 ). But patch clamping analysis showed that both depolarization-acti-
vated S-type anion currents and hyperpolarization-activated Ca 2 + currents are
impaired in atmrp5 mutant guard cells simultaneously (Suh et al. 2007 ), indicating
that AtMRP5 is a general regulator of ABA signaling rather than an ion channel.
To identify loci involved in ABA signaling, Erwin Grill's group screened a
large number of chemically mutagenized Arabidopsis seeds in the presence of
ABA, and 8 loci GCA1 to GCA8 (growth control exerted by ABA) were identi-
fied (Himmelbach et al. 1998 ). Further research found that two of them GCA1 and
GCA2 involve in ABA signaling in guard cells (Himmelbach et al. 1998 ). GCA2
was later found functioning upstream of ABA-induced ROS production, the activa-
tion of hyperpolarization-activated inward Ca 2 + channels, and cytosolic Ca 2 + ele-
vation in guard cells (Pei et al. 2000 ). Ca 2 + -imaging analysis showed that GCA2
involves in CO 2 - and ABA-induced stomatal closure by regulating the cytosolic
Ca 2 + oscillation pattern (Young et al. 2006 ; Allen et al. 2001 ). Recently, Ca 2 +
imaging and patch clamping analysis showed that ABA induces stomatal closure
in both Ca 2 + -dependent and Ca 2 + -independent manners, and GCA2 is important
for Ca 2 + -dependent ABA response for stomatal closure, not for Ca 2 + -independent
response (Siegel et al. 2009 ). Clearly, GCA2 is correlated to Ca 2 + and functions as
an important component for both ABA and CO 2 signaling in guard cells. However,
GCA2 has not been cloned so far. The genetic identification of GCA2 will facili-
tate our understanding about ABA signaling in guard cells.
ABA hypersensitive 1 ( abh1 ) is an ABA hypersensitive mutant which was iso-
lated in an Arabidopsis seed germination screening in the presence of 0.3 ΚΌ M
ABA, a concentration of ABA allowing wild-type seeds to germinate (Hugouvieux
et al. 2001 ). abh1 mutant shows an ABA hypersensitive phenotype in drought-
induced stomatal closure, but ABA content in leaves shows no significant
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