PubMed Health⌕ Search

PubMed · 16923015

Transcriptome profiling uncovers metabolic and regulatory processes occurring during the transition from desiccation-sensitive to desiccation-tolerant stages in Medicago truncatula seeds.

Abstract

To investigate regulatory processes and protective mechanisms leading to desiccation tolerance (DT) in seeds, 16086-element microarrays were used to monitor changes in the transcriptome of desiccation-sensitive 3-mm-long radicles of Medicago truncatula seeds at different time points during incubation in a polyethylene glycol (PEG) solution at -1.7 MPa, resulting in a gradual re-establishment of DT. Gene profiling was also performed on embryos before and after the acquisition of DT during maturation. More than 1300 genes were differentially expressed during the PEG incubation. A large number of genes involved in C metabolism are expressed during the re-establishment of DT. Quantification of C reserves confirms that lipids, starch and oligosaccharides were mobilised, coinciding with the production of sucrose during the early osmotic adjustment. Several clusters of gene profiles were identified with different time-scales. Genes expressed early during the PEG incubation belonged to classes involved in early stress and adaptation responses. Interestingly, several regulatory genes typically expressed during abiotic/drought stresses were also upregulated during maturation, arguing for the partial overlap of ABA-dependent and -independent regulatory pathways involved in both drought and DT. At later time points, in parallel to the re-establishment of DT, upregulated genes are comparable with those involved in late seed maturation. Concomitantly, a massive repression of genes belonging to numerous classes occurred, including cell cycle, biogenesis, primary and energy metabolism. The re-establishment of DT in the germinated radicles appears to concur with a partial return to the quiescent state prior to germination.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Julia Buitink, Jean J Leger, Isabelle Guisle, Benoit Ly Vu, Sylvie Wuillème, Guillaume Lamirault, Alice Le Bars, Nolwenn Le Meur, Anke Becker, Helge Küster, Olivier Leprince. 2006. Transcriptome profiling uncovers metabolic and regulatory processes occurring during the transition from desiccation-sensitive to desiccation-tolerant stages in Medicago truncatula seeds.. https://doi.org/10.1111/j.1365-313x.2006.02822.x

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

Ultraviolet-B-induced OsKOL4 promotes ABA accumulation by inhibiting OsABA8ox1 and OsABA8ox2 expression.

Ultraviolet-B (UV-B) light is a component of sunlight that influences plant survival and adaptation. UV-B induces plants to regulate their phenotypes and metabolism to increase resistance to UV-B and associated stresses. Abscisic acid (ABA) metabolism and signaling are important for plant responses to UV-B. However, the mechanisms underlying UV-B-induced ABA accumulation and signaling in rice remain poorly understood. Here, we report that ENT-KAURENE OXIDASE LIKE 4 (OsKOL4) regulates UV-B-induced responses and ABA biosynthesis. UV-B activates OsKOL4 expression via OsbZIP48, an ELONGATED HYPOCOTYL 5 (HY5) homolog that directly binds to the OsKOL4 promoter. Rice plants overexpressing OsKOL4 exhibit UV-B-induced phenotypes under normal conditions, along with ABA overaccumulation phenotypes resulting from increased ABA levels. Moreover, UV-B promotes ABA accumulation by inhibiting the expression of the ABA 8'-HYDROXYLASE1 and ABA 8'-HYDROXYLASE 2 (OsABA8ox1/2) genes through OsKOL4. OsKOL4 interacts with the transcription factor AP2/ERF ON CHROMOSOME 3 (OsAPE3), which in turn represses the transcription of OsABA8ox1/2. Furthermore, both UV-B and OsKOL4 enhance the binding of OsAPE3 to the OsABA8ox1/2 promoters. Collectively, our findings demonstrate that the OsKOL4-OsAPE3 module regulates ABA homeostasis in response to UV-B signaling by reducing ABA catabolism.

Abscisic Acid↗

From activation to desensitization: How ABA balances plant growth and abiotic stress response?

Abscisic acid (ABA) signaling is a central regulator of plant adaptation to abiotic stress, dynamically coordinating stress responses with growth and development. Rapid activation of ABA signaling promotes plant survival during the early stages of stress, whereas prolonged stress requires timely attenuation of the pathway to restore growth and prevent excessive stress responses. Recent studies have uncovered diverse mechanisms underlying ABA desensitization, including regulation of SnRK2 kinases, phytohormone crosstalk, nutrient signaling, protein trafficking, post-translational modifications, and feedback regulatory networks. Together, these interconnected mechanisms enable plants to fine-tune ABA signaling in response to developmental and environmental cues. In this review, we summarize recent advances in understanding the molecular mechanisms that attenuate ABA signaling and restore the balance between growth and stress adaptation during prolonged stress. We also highlight outstanding questions and discuss strategies for engineering ABA signaling dynamics to improve crop resilience, productivity, and adaptation to increasingly variable environments.

Abscisic Acid↗

The effect of heat shock on paclitaxel production in Taxus yunnanensis cell suspension cultures: role of abscisic acid pretreatment.

The heat shock (HS) response is a conserved cellular defense mechanism to elevated temperatures, observed in cells from bacteria to human. It is characterized by the increased accumulation of HS proteins. This work examines the effect of HS on the secondary metabolite biosynthesis of cultured plant cells. Suspension cultures of Taxus yunnanensis cells, which produce the anticancer diterpenoid paclitaxel (Taxol), were heat shocked at 35-50 degrees C for 30-60 min. The results show that HS reduced cell viability and growth but significantly induced paclitaxel production. The HS-induced paclitaxel production depended on the intensity of HS and the physiological state of the cells. Abscisic acid (ABA)-pretreatment not only increased cell viability and growth upon HS but also improved HS-induced paclitaxel yield. The best culture phase to apply the HS was the late-exponential growth phase. Under the optimized condition, HS enhanced paclitaxel yield by sixfold to 6.8 mg/L. In addition, a prior mild-HS treatment also significantly increased HS-induced paclitaxel production. Furthermore, HS induced oxidative burst, the early event of plant defense response to pathogen attack and other stress challenge; the addition of putative inhibitors of lipoxygenase, a key enzyme for jasmonic acid biosynthesis, significantly inhibited HS-induced pacliatxel accumulation. The stimulation of secondary metabolite production by HS may be a result of HS-induced plant cell defense response.

Abscisic Acid↗