User:M6zakh/sandbox

= Guard cell = From Wikipedia, the free encyclopedia Opening and Closing of Stoma. A stomatal pore in the surface (epidermis) of a leaf as viewed through a microscope. The central stomatal pore is formed by a pair of guard cells. The stomatal pore can either open (left) or close (right) depending on the environmental conditions.

Guard cells are specialized cells in the epidermis of leaves, stems and other organs that are used to control gas exchange during transpiration. They are produced in pairs with a gap between them that forms a stomatal pore. The stomatal pores are largest when water is freely available and photorespiration is occurring. This causes the guard cells become turgid. Stomatal pores close when water availability is critically low and photorespiration is cased which in turn causes the guard cells to become flaccid. Photosynthesis depends on the diffusion of carbon dioxide (CO2) from the air through the stomata into the mesophyll tissues. Oxygen (O2), produced as a byproduct of photosynthesis, exits the plant via the stomata. When the stomata are open, water is lost by evaporation and must be replaced via the transpiration stream, with water taken up by the roots. Plants must balance the amount of CO2 absorbed from the air with the water loss through the stomatal pores during transpiration, and this is achieved by both active and passive control of guard cell turgor and stomatal pore size.

Guard cell function[edit]
Guard cells contain phototropins which are serine and threonine kinases mediated by light. They contain two light, oxygen, and voltage (LOV) domains, and are also part of the PAS domain superfamily. These phototropins trigger many responses such as phototropism, chloroplast movement, leaf expansion, and stomatal opening. Light is the main trigger for the opening or closing of stomata. Not much was previously known on how the photoreceptors work. To understand the mechanism to which phototropins work, an experiment on broad bean (Vicia faba) was done. Immunodetection and far-western blot analysis was used to determine blue light excites phototropin 1 and phototropin 2, which causes protein phosphate 1 to begin a phosphorylation cascade, which activates H+-ATPase, a pump responsible for pumping H+ ions out of the cell. The phosphorylated H+-ATPase allows the binding of a 14-3-3 protein, an autoinhibitory domain of H+-ATPase, to the C terminus. Serine and threonine are then phosphorylated within the protein, which induces H+-ATPase activity. The same experiment also found that upon phosphorylation, a 14-3-3 protein was bound to the phototropins before the H+-ATPase had been phosphorylated. . In a similar experiment they concluded that the binding of 14-3-3 protein to the phosphorylation site is essential to the activation of plasma membrane H+-ATPase activity. This was done by adding phosphopeptides such as P-950, which inhibits the binding of 14-3-3 protein, to phosphorylated H+-ATPase and observing the amino acid sequence. As protons are being pumped out, a negative electrical potential within the plasma membrane is formed. This hyperpolarization of the membrane allows for the accumulation of positively charged potassium (K+) ions and chloride (Cl−) ions, which in turn, increases the solute concentration causing the water potential to decrease. The negative water potential allows for osmosis to occur in the guard cell, allowing the cell to become turgid. Opening and closure of the stomatal pore is mediated by changes in the turgor pressure of the two guard cells.The turgor pressure of guard cells is controlled by movements of large quantities of ions and sugars into and out of the guard cells. Guard cells have cell walls of varying thickness and differently oriented cellulose microfibers, causing them to bend outward when they are turgid, which in turn, causes stomata to open. Stomata close when there is an osmotic loss of water, occurring from the loss of K+ to neighboring cells.