Auxin-binding-protein antibodies and peptides influence stomatal opening

 

 

Auxin-binding-protein antibodies and peptides influence stomatal opening and alter cytoplasmic pH

by Gehring C. A., McConchie R. M., Venis M. A., Parish R. W. (1998)

Robyn_Mcconchie
Robyn McConchie, University of Sydney, Australia
Roger_Parish
Roger Parish, La Trobe University, Melbourne, Australia

Department of Botany, La Trobe University, Bundoora, Victoria, Australia.

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in Planta 205: 581-586 – DOI: 10.1007/s004250050359 –

https://www.ncbi.nlm.nih.gov/pubmed/9684362

Abstract

Previous work has shown that stomatal opening induced by indole-3-acetic acid (IAA) in epidermal strips of the orchid Paphiopedilum tonsum L. is preceded by a reduction in cytoplasmic pH (pHi) of the guard cells.

We now report that Fab fragments of an auxin-agonist antibody (D16), directed against a putative auxin-binding domain of the auxin-binding protein ABP1, induce stomatal opening and decrease guard-cell pHi, as monitored with the acetomethoxy ester of the ratiometric pH indicator Snarf-1.

Similar activity was shown by a monoclonal antibody against the same domain. The C-terminal dodecapeptide, Pz152-163 of maize ABP1 (ABPzm1) induced guard-cell alkalinization and closed stomata, as did Fab fragments of a monoclonal antibody (MAC 256) recognising the C-terminal region of ABPzm1.

By implicating, for the first time, an auxin-binding protein in mediation of an auxin-dependent physiological response, these findings strongly support an auxin-receptor role for ABP1.

Stomata responses to kinetin and natriuretic peptides

 

Stomatal guard cell responses to kinetin and natriuretic peptides are cGMP-dependent

by Pharmawati M., Billington T., Gehring C. A. (1998)

made_pharmawati
Made Pharmawati, Udayana University, Badung

 

Billington T.

 

gehring_100x100
Catherine A. Gehring, Northern Arizona University, USA

in Cell. Mol. Life Sci. 54, 272–276. – doi: 10.1007/s000180050149 –

PubMed Abstract | CrossRef Full Text | Google Scholar – 

http://link.springer.com/article/10.1007%2Fs000180050149

Abstract

Immunological evidence suggests that plants contain natriuretic peptides (NPs) and furthermore (3- [125I]iodotyrosol28) rat atrial NP (rANP) binds specifically to plant membranes. rANP and immunoaffinity-purified plant NP analogues also promote concentration-dependent stomatal opening.

Here we report that kinetin, a synthetic cytokinin, and rANP induce stomatal opening in Tradescantia albiflora and that the effect of rANP is critically dependent on the secondary structure of the peptide hormone. The native circular molecule is active, whereas the linearized molecule shows no biological activity.

Furthermore, kinetin- and rANP-induced stomatal opening is reversibly inhibited by two in hibitors of guanylate cyclase, LY 83583 and methylene blue.

Stomatal opening is also induced in a concentration-dependent manner by the cell-permeant cyclic guanosine-3′,5′-monophosphate (cGMP) analogue 8-Br-cGMP, and this effect is prevented by the stomatal closure promoting plant hormone abscisic acid (ABA).

We conclude that in guard cells kinetin and rANP pathways operate via guanylate cyclase upregulation, and we propose that ABA-induced closure is not cGMP-dependent.

Stomatal movements, pH and Ca.

 

Changes in cytoplasmic pH and calcium in guard cells precede stomatal movements.

by Irving H. R., Gehring C. A., Parish R. W. (1992)

in Proc. Natl Acad. Sci. USA, 89, 17901794. – 

CrossRef |PubMed | [PMC free article]

Abstract

Stomatal opening is induced by indoleacetic acid (IAA), cytokinins, and fusicoccin (FC), whereas stomatal closure is induced by abscisic acid (ABA).

To test the effect of these growth regulators on guard cell cytosolic Ca2+ ([Ca2+]cyt) and pH (pHcyt), epidermal strips were taken from the lower side of leaves of the orchid Paphiopedilum tonsum and were loaded with acetomethoxy-esterified forms of the Ca2+ indicator fluo-3 or the pH indicator 2′,7′-bis(2-carboxyethyl)-5(6)carboxyfluorescein.

Basal [Ca2+]cyt ranged from 0.05 to 0.3 M and was 0.22 +/- 0.015 (n = 21). Increases in both [Ca2+]cyt and pHcyt were observed in guard cells after application of 10-100 M ABA to open stomata, and these preceded stomatal closure.

The increase in [Ca2+]cyt ranged from 1.5- to 3-fold and was seen in 7 of 10 experiments. Guard cell alkalinization began within 2 min of ABA treatment and continued for the next 8 min. The increase ranged from 0.04 to 0.3 pH unit and was seen in 13 of 14 experiments. Guard cell [Ca2+]cyt increased, whereas pHcyt decreased after treatment of closed stomata with IAA, kinetin, or FC.

In response to 50-100 M IAA, [Ca2+]cyt increased 1.5- to 2-fold in all cases, and pHcyt decreased 0.2-0.4 unit within 5 min in 7 experiments. Within 12 min, 10-100 M kinetin caused [Ca2+]cyt to increase in 28 of 34 experiments (1.3- to 2.5-fold) and pHcyt fell 0.1-0.4 unit in 15 of 17 treatments. The response to 10-50 M FC was similar in both time and magnitude.

These results show that stomatal opening is accompanied by an increase in [Ca2+]cyt and cytosolic acidification in the guard cells, whereas stomatal closure is preceded by an increase in [Ca2+]cyt and cytosolic alkalinization in the guard cells. The order of these events is still uncertain, but changes in pHcyt are correlated with stomatal movement, and these changes may be an important factor in the regulation of guard cell movement.

Stomata, auxins, peptides and pH

 

 

Auxin-binding-protein antibodies and peptides influence stomatal opening and alter cytoplasmic pH

by Gehring C. A., McConchie R. M., Venis M. A., Parish R. W. (1998)

in Planta June 1998, Volume 205, Issue 4, pp 581-586 – 

http://link.springer.com/article/10.1007/s004250050359

Abstract.

Previous work has shown that stomatal opening induced by indole-3-acetic acid (IAA) in epidermal strips of the orchid Paphiopedilum tonsum L. is preceded by a reduction in cytoplasmic pH (pHi) of the guard cells.

We now report that Fab fragments of an auxin-agonist antibody (D16), directed against a putative auxin-binding domain of the auxin-binding protein ABP1, induce stomatal opening and decrease guard-cell pHi, as monitored with the acetomethoxy ester of the ratiometric pH indicator Snarf-1.

Similar activity was shown by a monoclonal antibody against the same domain. The C-terminal dodecapeptide, Pz152–163 of maize ABP1 (ABPzm1) induced guard-cell alkalinization and closed stomata, as did Fab fragments of a monoclonal antibody (MAC 256) recognising the C-terminal region of ABPzm1.

By implicating, for the first time, an auxin-binding protein in mediation of an auxin-dependent physiological response, these findings strongly support an auxin-receptor role for ABP1.