Over the past years we have been involved in a forward genetic screen aiming at identification of gas exchange mutants. 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.
Among mutants that often phenocopy stomatal mutants are those impaired in synthesis of leaf epidermal cuticle, or establishment of epidermal cell adhesion. Because of the loss of epidermal barriers to water vapor, such mutants exhibit elevated loss of water from detached leaves.
We map and characterize the cell adhesion mutants to broaden the landscape of genetic factors affecting cell adhesion.
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.
Guard cell signaling, along with cuticle impermeable to water vapor, and tight adhesion between epidermal pavement cells are crucial to restrict uncontrolled transpiration.
However, 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.