PubMed Health⌕ Search

PubMed · 8347670

Abscisic acid-lipid interactions: a phospholipid monolayer study.

Abstract

Lipid monolayer studies were performed on a Langmuir trough in the absence and in the presence of the plant hormone abscisic acid (ABA). The ABA-induced effects on the lipid monolayers can be summarized as follows: (i) ABA as the free acid (pH below 5.3) increased the molecular area and slightly decreased the surface pressure in the collapse points of monolayers made of saturated, unsaturated and of mixed lipids; ABA as the anion showed only minor effects. (ii) The ABA-induced area increase of the lipid monolayers decreased when the surface pressure increased, but some ABA remained in the monolayers made of unsaturated phospholipids even at collapse pressure. (iii) The incorporation of ABA into the monolayers could be inhibited by adding the plant sterol beta-sitosterol to the monolayer forming phospholipids. (iv) There was no substantial difference of ABA action on plant phospholipids as compared with other phospholipids. (v) ABA had a much stronger influence on unsaturated phospholipids than on saturated ones. (vi) ABA decreased the phase-transition temperature of saturated phospholipids. These results, which agree with those obtained from phospholipid vesicle studies, indicate that the physical state of the lipid is important for the ability of ABA penetrating into the lipid monolayer. Finally, a possible relevance of these results is discussed in terms of the action of ABA on guard cell membranes of plants.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

H Bürner, R Benz, H Gimmler, W Hartung, W Stillwell. 1993-08-15. Abscisic acid-lipid interactions: a phospholipid monolayer study.. https://doi.org/10.1016/0005-2736(93)90086-f

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↗