Glasgow Theses Service

Membrane and ion channel trafficking in stomatal regulation

Eisenach, Cornelia (2011) Membrane and ion channel trafficking in stomatal regulation. PhD thesis, University of Glasgow.

Due to Embargo and/or Third Party Copyright restrictions, this thesis is not available in this service.

Abstract

Stomata open in response to light allowing CO2 uptake for photosynthesis and they close in response to abiotic stress, such as drought, to prevent transpirational water loss from the plant. A pair of guard cells surrounds each stoma and stomatal movements depend on K+ fluxes across the guard cell plasma membrane. These fluxes are mediated by inward and outward rectifying K+ channels (K+in and K+out). The SNARE SYP121 was originally identified in association with ion channel regulation in guard cells. SNARE proteins mediate vesicle fusion and facilitate delivery of membrane proteins to target membranes. They are also linked to a variety of physiological responses. In particular, the plasma membrane SNARE SYP121 has been attributed a role in immune response and K+ nutrition. I have used the Arabdopsis loss-of-function mutant syp121 and uncovered a set of mutant phenotypes associated with impaired stomatal opening. In the syp121 mutant stomatal reopening was delayed and incomplete following Ca2+-induced closure, and increase in stomatal transpiration was slowed in the light. Incomplete reopening was rescued by complementation with wild-type SYP121 and was not observed in the syp122 mutant, lacking the homologous gene product. Guard cell K+ in current, necessary for K+ uptake during stomatal reopening, was reduced in syp121 mutant guard cells. Analysis of current gating characteristics suggested an impaired delivery of K+in channels to the plasma membrane, which was consistent with inhibition of stomatal reopening by the trafficking inhibitor Brefeldin A in wild-type plants. Impaired stomatal reopening in the syp121 mutant was phenomenologically similar to a Ca2+-encoded form of ‘programmed closure’ and my results suggest that endocytosis and delayed recycling of K+in channels may underly this phenomenon. Impaired stomatal function manifested in a conditional syp121 mutant growth phenotype dependent on high light and low humidity, characterised by reduced stomatal conductance and photosynthetic CO2 assimilation. My results suggested the necessity for SYP121-dependent K+in channel traffic during stomatal reopening. My results revealed a novel syp121 stomatal phenotype that was linked to K+in channel recycling in guard cells and had consequences for whole-plant water use and biomass production.

Item Type: Thesis (PhD)
Qualification Level: Doctoral
Additional Information: Due to copyright restrictions the full text of this thesis cannot be made available online. Access to the printed version is available once any embargo periods have expired.
Keywords: Guard cell, ion channel, K+ channel, trafficking, SNARE, SYP121
Subjects: Q Science > QK Botany
Q Science > Q Science (General)
Colleges/Schools: College of Medical Veterinary and Life Sciences > Institute of Molecular Cell and Systems Biology
Supervisor's Name: Blatt, Prof. M.R.
Date of Award: 2011
Embargo Date: 7 November 2014
Depositing User: Ms Cornelia Eisenach
Unique ID: glathesis:2011-3004
Copyright: Copyright of this thesis is held by the author.
Date Deposited: 14 Nov 2011
Last Modified: 10 Dec 2012 14:02
URI: http://theses.gla.ac.uk/id/eprint/3004

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