1. Stomatal transpiration is regulated by the turgidity of guard cells.
2. Turgor pressure, acting on the unevenly thickened guard cell wall, governs stomatal movement.
3. The elastic outer wall stretches, pulling the inner inelastic wall, causing stomatal opening.
4. Flaccidity of guard cells results in stomatal closure.
5.Osmotically active sugar increases guard cell osmotic potential, leading to stomatal opening.
6. Nighttime starch formation causes guard cells to lose water, leading to stomatal closure.
7. Lloyd (1908) found starch in guard cells. According to the starch-sugar hypothesis, guard cells use starch in photosynthesis during the day, raising the pH (7.0). Active phosphorylase converts starch to glucose-1-phosphate, increasing DPD and making cells turgid, opening stomata. At night, photosynthesis stops, and starch accumulates, lowering pH (5.0). Glucose-1-phosphate turns into starch, reducing DPD, and causing flaccidity, leading to stomatal closure.
Starch + iP → Glucose – 1 – phosphate
8.Stomatal opening results from the accumulation of potassium ions in guard cells, increasing solute potential and causing water to enter, making the cells turgid and leading to pore opening. Conversely, stomatal closing happens when water is removed, making guard cells flaccid. Removal of K+ ions causes the pore to close, typically occurring in the dark or during low photosynthesis rates.