While stomatal closure clearly did not prevent disease infection by the rusts, like Bgh, has obvious and serious implications for physiological activity mediated by stomatal movement. 1 and 2) show low g l, indicating failure of stomatal opening in light, until the epidermis was ruptured some time after infection. Although these rusts are also obligate biotrophs, they enter leaves via stomata and feed largely on mesophyll cells before rupturing the epidermis at the onset of sporulation. In line with earlier studies of bean rust, 5 we recently found a very similar effect of infection by brown rust fungi in susceptible barley (cv. Our observations of compatible interactions confirmed earlier studies 4 showing that stomata in the vicinity of established colonies lost the ability to open in response to light, thus reducing leaf water conductance ( g l). hordei ( Bgh), 3 but as Bgh does not enter via stomata, the effect, if any, of this closure on the pathogen is not direct.īgh is an obligate biotroph with an ectophytic habit it penetrates only into epidermal cells to form feeding structures (haustoria) that supply the surface mycelia and reproductive structures. Our published study showed that rapid stomatal closure is also a pre-penetration response of barley to the powdery mildew fungus, Blumeria graminis f. 2 showed that bacterial pathogen-associated molecular patterns trigger rapid stomatal closure, and argued that this represents an innate mechanism of resistance against pathogens that enter via stomatal pores. Stomata balance CO 2 uptake with transpiration1 in response to physiological and environmental cues and they also respond to biotic stress including pathogen attack.
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