IIB   20738
INSTITUTO DE INVESTIGACIONES BIOLOGICAS
Unidad Ejecutora - UE
artículos
Título:
Nitric Oxide Triggers Phosphatidic Acid Accumulation via Phospholipase D during Auxin-Induced Adventitious
Autor/es:
LANTERI, L.; LAXALT, A. M.; LAMATTINA, L
Revista:
PLANT PHYSIOLOGY.
Editorial:
American Society of Plant Biologists (ASPB)
Referencias:
Año: 2008 vol. 147 p. 188 - 198
ISSN:
0032-0889
Resumen:
Auxin and nitric oxide (NO) play fundamental roles throughout plant life. NO is a second messenger in auxin signal transduction
leading to root developmental processes. The mechanisms triggered by auxin and NO that direct adventitious root (AR)
formation are beginning to be unraveled. The goal of this work was to study phospholipid (PL) signaling during the auxin- and
NO-induced AR formation in cucumber (Cucumis sativus) explants. Explants were labeled with 32P-inorganic phosphate and
treated with the auxins indole-3-acetic acid or 1-naphthylacetic acid, or the NO donor S-nitroso N-acetyl penicillamine, in the
presence or absence of the specific NO scavenger 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide. PLs were
separated by thin-layer chromatography and quantified. We report that the signaling PLs phosphatidic acid (PA), phosphatidylinositol
phosphate, and phosphatidylinositol bisphosphate accumulated within 1 min after auxin or NO treatment. Both
auxin and NO evoked similar and transient time course responses, since signaling PLs returned to control levels after 20 or
30 min of treatment. The results indicate that auxin relies on NO in inducing PA, phosphatidylinositol phosphate, and
phosphatidylinositol bisphosphate accumulation. Furthermore, we demonstrate that auxin and NO trigger PA formation via
phospholipase D (PLD) activity. Explants treated for 10 min with auxin or NO displayed a 200% increase in AR number
compared with control explants. In addition, PLD activity was required for the auxin- and NO-induced AR formation. Finally,
exogenously applied PA increased up to 300% the number of ARs. Altogether, our data support the idea that PLD-derived PA is
an early signaling event during AR formation induced by auxin and NO in cucumber explants.
presence or absence of the specific NO scavenger 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide. PLs were
separated by thin-layer chromatography and quantified. We report that the signaling PLs phosphatidic acid (PA), phosphatidylinositol
phosphate, and phosphatidylinositol bisphosphate accumulated within 1 min after auxin or NO treatment. Both
auxin and NO evoked similar and transient time course responses, since signaling PLs returned to control levels after 20 or
30 min of treatment. The results indicate that auxin relies on NO in inducing PA, phosphatidylinositol phosphate, and
phosphatidylinositol bisphosphate accumulation. Furthermore, we demonstrate that auxin and NO trigger PA formation via
phospholipase D (PLD) activity. Explants treated for 10 min with auxin or NO displayed a 200% increase in AR number
compared with control explants. In addition, PLD activity was required for the auxin- and NO-induced AR formation. Finally,
exogenously applied PA increased up to 300% the number of ARs. Altogether, our data support the idea that PLD-derived PA is
an early signaling event during AR formation induced by auxin and NO in cucumber explants.
treated with the auxins indole-3-acetic acid or 1-naphthylacetic acid, or the NO donor S-nitroso N-acetyl penicillamine, in the
presence or absence of the specific NO scavenger 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide. PLs were
separated by thin-layer chromatography and quantified. We report that the signaling PLs phosphatidic acid (PA), phosphatidylinositol
phosphate, and phosphatidylinositol bisphosphate accumulated within 1 min after auxin or NO treatment. Both
auxin and NO evoked similar and transient time course responses, since signaling PLs returned to control levels after 20 or
30 min of treatment. The results indicate that auxin relies on NO in inducing PA, phosphatidylinositol phosphate, and
phosphatidylinositol bisphosphate accumulation. Furthermore, we demonstrate that auxin and NO trigger PA formation via
phospholipase D (PLD) activity. Explants treated for 10 min with auxin or NO displayed a 200% increase in AR number
compared with control explants. In addition, PLD activity was required for the auxin- and NO-induced AR formation. Finally,
exogenously applied PA increased up to 300% the number of ARs. Altogether, our data support the idea that PLD-derived PA is
an early signaling event during AR formation induced by auxin and NO in cucumber explants.
presence or absence of the specific NO scavenger 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide. PLs were
separated by thin-layer chromatography and quantified. We report that the signaling PLs phosphatidic acid (PA), phosphatidylinositol
phosphate, and phosphatidylinositol bisphosphate accumulated within 1 min after auxin or NO treatment. Both
auxin and NO evoked similar and transient time course responses, since signaling PLs returned to control levels after 20 or
30 min of treatment. The results indicate that auxin relies on NO in inducing PA, phosphatidylinositol phosphate, and
phosphatidylinositol bisphosphate accumulation. Furthermore, we demonstrate that auxin and NO trigger PA formation via
phospholipase D (PLD) activity. Explants treated for 10 min with auxin or NO displayed a 200% increase in AR number
compared with control explants. In addition, PLD activity was required for the auxin- and NO-induced AR formation. Finally,
exogenously applied PA increased up to 300% the number of ARs. Altogether, our data support the idea that PLD-derived PA is
an early signaling event during AR formation induced by auxin and NO in cucumber explants.
Cucumis sativus) explants. Explants were labeled with 32P-inorganic phosphate and
treated with the auxins indole-3-acetic acid or 1-naphthylacetic acid, or the NO donor S-nitroso N-acetyl penicillamine, in the
presence or absence of the specific NO scavenger 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide. PLs were
separated by thin-layer chromatography and quantified. We report that the signaling PLs phosphatidic acid (PA), phosphatidylinositol
phosphate, and phosphatidylinositol bisphosphate accumulated within 1 min after auxin or NO treatment. Both
auxin and NO evoked similar and transient time course responses, since signaling PLs returned to control levels after 20 or
30 min of treatment. The results indicate that auxin relies on NO in inducing PA, phosphatidylinositol phosphate, and
phosphatidylinositol bisphosphate accumulation. Furthermore, we demonstrate that auxin and NO trigger PA formation via
phospholipase D (PLD) activity. Explants treated for 10 min with auxin or NO displayed a 200% increase in AR number
compared with control explants. In addition, PLD activity was required for the auxin- and NO-induced AR formation. Finally,
exogenously applied PA increased up to 300% the number of ARs. Altogether, our data support the idea that PLD-derived PA is
an early signaling event during AR formation induced by auxin and NO in cucumber explants.
presence or absence of the specific NO scavenger 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide. PLs were
separated by thin-layer chromatography and quantified. We report that the signaling PLs phosphatidic acid (PA), phosphatidylinositol
phosphate, and phosphatidylinositol bisphosphate accumulated within 1 min after auxin or NO treatment. Both
auxin and NO evoked similar and transient time course responses, since signaling PLs returned to control levels after 20 or
30 min of treatment. The results indicate that auxin relies on NO in inducing PA, phosphatidylinositol phosphate, and
phosphatidylinositol bisphosphate accumulation. Furthermore, we demonstrate that auxin and NO trigger PA formation via
phospholipase D (PLD) activity. Explants treated for 10 min with auxin or NO displayed a 200% increase in AR number
compared with control explants. In addition, PLD activity was required for the auxin- and NO-induced AR formation. Finally,
exogenously applied PA increased up to 300% the number of ARs. Altogether, our data support the idea that PLD-derived PA is
an early signaling event during AR formation induced by auxin and NO in cucumber explants.
S-nitroso N-acetyl penicillamine, in the
presence or absence of the specific NO scavenger 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide. PLs were
separated by thin-layer chromatography and quantified. We report that the signaling PLs phosphatidic acid (PA), phosphatidylinositol
phosphate, and phosphatidylinositol bisphosphate accumulated within 1 min after auxin or NO treatment. Both
auxin and NO evoked similar and transient time course responses, since signaling PLs returned to control levels after 20 or
30 min of treatment. The results indicate that auxin relies on NO in inducing PA, phosphatidylinositol phosphate, and
phosphatidylinositol bisphosphate accumulation. Furthermore, we demonstrate that auxin and NO trigger PA formation via
phospholipase D (PLD) activity. Explants treated for 10 min with auxin or NO displayed a 200% increase in AR number
compared with control explants. In addition, PLD activity was required for the auxin- and NO-induced AR formation. Finally,
exogenously applied PA increased up to 300% the number of ARs. Altogether, our data support the idea that PLD-derived PA is
an early signaling event during AR formation induced by auxin and NO in cucumber explants.