Research

Stomata are epidermal pores surrounded by pairs of guard cells that balance transpiration and uptake of CO2 for photosynthesis. Guard cells respond to multiple environmental factors, e.g., light, leaf internal CO2 concentration, drought, low air humidity, pathogens and air pollutants such as ozone (O3), to optimize CO2 uptake and control water loss, or prevent the entry of pathogens into the leaf tissue. Mechanically, opening and closing of stomatal pores is achieved through changes in guard cell volume and turgor pressure which in turn are regulated by the activity of multiple ion channels localized (mostly) at the guard cell plasma membrane.

Over the past years we have been involved in a forward genetic screen aiming at saturation of guard cell signaling network. Surprisingly, multiple mutants identified during this project are not impaired in stomatal movements. These, non-trivial mutants, depending on the assay used, can phenocopy stomatal mutants and are the major interest of our group.

Learning from non-trivial mutants

Among mutants that often phenocopy stomatal mutants are those impaired in synthesis of leaf epidermal cuticle, or establishment of epidermal cell adhesion (see below). Because of the loss of epidermal barriers to water vapor, such mutants exhibit elevated loss of water from detached leaves.

The above mentioned classes of mutants represent the great majority of processes controlling uncontrolled transpiration, but do not fully saturate the genetic landscape.

We recently characterized a cell wall mutant exhibiting high loss of water from detached leaves that can not be explained by the loss of cell adhesion, impaired cuticule deposition, or inability to close stomata. We continue to work on this problem with the aim to expand the current models of plant gas exchange.