Transcriptional regulatory network triggered by oxidative signals configures the early response mechanisms of japonica rice to chilling stress
K.Y. Yun, M.R. Park, B. Mohanty, V. Herath, F. Xu, R. Mauleon, E. Wijaya, V.B. Bajic, R. Bruskiewich, B.G. de Los Reyes
BMC Plant Biol., 10:16, (2010)
Transcriptional regulatory network
The transcriptional regulatory network involved in low temperature response leading to acclimation has been established in Arabidopsis.
In japonica rice, which can only withstand transient exposure to milder
cold stress (10°C), an oxidative-mediated network has been proposed to
play a key role in configuring early responses and short-term defenses.
The components, hierarchical organization and physiological consequences
of this network were further dissected by a systems-level approach.
Regulatory clusters responding directly
to oxidative signals were prominent during the initial 6 to 12 hours at
10°C. Early events mirrored a typical oxidative response based on
striking similarities of the transcriptome to disease, elicitor and
wounding induced processes. Targets of oxidative-mediated mechanisms are
likely regulated by several classes of bZIP factors acting on
as1/ocs/TGA-like element enriched clusters, ERF factors acting on
GCC-box/JAre-like element enriched clusters and R2R3-MYB factors acting
on MYB2-like element enriched clusters.
Temporal induction of several H2O2-induced bZIP, ERF and MYB genes coincided with the transient H2O2 spikes within the initial 6 to 12 hours. Oxidative-independent responses involve DREB/CBF, RAP2 and RAV1
factors acting on DRE/CRT/rav1-like enriched clusters and bZIP factors
acting on ABRE-like enriched clusters. Oxidative-mediated clusters were
activated earlier than ABA-mediated clusters.
Genome-wide, physiological and
whole-plant level analyses established a holistic view of chilling
stress response mechanism of japonica rice. Early response regulatory
network triggered by oxidative signals is critical for prolonged
survival under sub-optimal temperature. Integration of stress and
developmental responses leads to modulated growth and vigor maintenance
contributing to a delay of plastic injuries.
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