West Lafayette, Indiana
March 11, 2009
Purdue University researchers have determined a process that
regulates activity of genes that control seed germination and
seedling development.
 Mike
Hasegawa (photo), the Bruno C. Moser Distinguished Professor of
Horticulture and Landscape Architecture, and Kenji Miura, a
former Purdue postdoctoral researcher and now an assistant
professor at Tsukuba
University in Japan, discovered the step involved in keeping
seeds from germinating in adverse conditions such as freezing
temperatures or drought, a factor in the survival of plant
species.
The work, which was published today in the early online version
of the Proceedings of the National
Academy of Sciences, is part of ongoing research that has
uncovered that similar processes affects a plant's freeze
tolerance and absorption of phosphate.
"We've found the process, called sumoylation, is involved in the
regulation of some major agricultural traits," Hasegawa said.
"It is fundamental, basic research like this that allows us to
understand how plants respond to hormones and environmental
conditions."
Seeds produce a hormone called abscisic acid, or ABA, that
prevents germination. When environmental factors such as
temperature are not optimal for seed germination, ABA levels are
high, which causes production of higher levels of a protein
called ABI5. When the ABI5 protein is active, it switches on
genes that prevent germination.
Hasegawa's research showed that when a SUMO peptide is attached
to the ABI5 protein, the protein becomes inactive, switching off
the genes that prevent germination and seedling development.
"A single stimulus such as ABA affects transcription factors,
which are major controllers of genes involved in complex
processes such as seed germination," Hasegawa said. "Sumoylation
seems to be an important process in the control of significant
plant characteristics."
Hasegawa said that the ABI5 protein can become active again,
halting germination and seedling development if condition are no
longer optimal. When conditions change to make plant development
possible, the protein can once again be deactivated.
The National Science Foundation and the U.S. Department of
Agriculture have funded the research in Hasegawa's laboratory.
Hasegawa's next step is to determine how the sumoylation process
leads to gene suppression and expression.
ABSTRACT
Sumoylation of ABI5 by
the Arabidopsis SUMO E3 Ligase SIZ1 Negatively Regulates
Abscisic Acid Signaling
Kenji Miura, Jiyoung Lee, Jing Bo Jin, Chan Yul Yoo,
Tomoko Miura, and Paul M. Hasegawa
SUMO (small ubiquitin-related modi?er) conjugation (i.e.,
sumoylation) to protein substrates is a reversible
posttranslational modi?cation that regulates signaling by
modulating transcription factor activity. This paper
presents evidence that the SUMO E3 ligase SIZ1 negatively
regulates abscisic acid (ABA) signaling, which is dependent
on the bZIP transcription factor ABI5. Loss-of-function
T-DNA insertion siz1–2 and siz1–3 mutations caused ABA
hypersensitivity for seed germination arrest and seedling
primary root growth inhibition. Furthermore, expression of
genes that are ABA-responsive through ABI5-dependent
signaling (e.g., RD29A, Rd29B, AtEm6, RAB18, ADH1) was
hyperinduced by the hormone in siz1 seedlings. abi5– 4
suppressed ABA hypersensitivity caused by siz1 (siz1–2 abi5–
4), demonstrating an epistatic genetic interaction between
SIZ1 and ABI5. A K391R substitution in ABI5 [ABI5(K391R)]
blocked SIZ1-mediated sumoylation of the transcription
factor in vitro and in Arabidopsis protoplasts, indicating
that ABI5 is sumoylated through SIZ1 and that K391 is the
principal site for SUMO conjugation. In abi5– 4 plants,
ABI5(K391R) expression caused greater ABA hypersensitivity
(gene expression, seed germination arrest and primary root
growth inhibition) compared with ABI5 expression. Together,
these results establish that SIZ1-dependent sumoylation of
ABI5 attenuates ABA signaling. The double mutant siz1–2
afp-1 exhibited even greater ABA sensitivity than the single
mutant siz1, suggesting that SIZ1 represses ABI5 signaling
function independent of AFP1.
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