Eczematous (irritant and allergic) reactions of the skin and barrier function as determined by water vapour loss

The aim of this study was to compare the influence of irritant and allergic reactions on the barrier function of the skin and to correlate disturbances of barrier function with macroscopically visible changes. For this purpose, the skin of the volar side of the forearm was exposed to nickel sulphate (5%), sodium lauryl sulphate (5%), dimethyl sulphoxide (50%) and phenol (5%) during a period of 48 h. Distilled water served as control. The exposures were made in a test panel of 23 female subjects consisting of a group of 14 patients with positive skin reactions to nickel sulphate and nine controls in whom no evidence of skin disease was found. Both skin water vapour loss measurements and a ‘visual scoring sytem’ (based on erythema, fissuring and scaling) were used to assess the effects of the substances on the skin. The test sites exposed to nickel sulphate were also read for allergic reactions. In both groups all test substances caused an increase in skin water vapour loss in comparison with distilled water. The increase was found to be statistically significant for nickel sulphate, sodium laury I sulphate and dimethyl sulphoxide (α= 0·05). Erythema was consistently elicited by the test substances, particularly by sodium lauryl sulphate. In addition, dimethyl sulphoxide regularly caused fine cracks (chapping). The correlation between erythema and the increase in water vapour loss after exposure of the skin to an irritant varied considerably from substance to substance and was poor for nickel sulphate (5%) and phenol (5%) and negative for dimethyl sulphoxide (50%). A significant correlation was found for sodium lauryl sulphate (5%). This implies that a linear relationship between barrier function impairment and damage to the viable cells of deeper layers of the skin may not be assumed beforehand

Visualization of BRI1 and BAK1(SERK3) membrane receptor heterooligomers during brassinosteroid signaling.

The leucine-rich repeat receptor-like kinase BRASSINOSTEROID-INSENSITIVE1 (BRI1) is the main ligand-perceiving receptor for brassinosteroids (BRs) in Arabidopsis (Arabidopsis thaliana). Binding of BRs to the ectodomain of plasma membrane (PM)-located BRI1 receptors initiates an intracellular signal transduction cascade that influences various aspects of plant growth and development. Even though the major components of BR signaling have been revealed and the PM was identified as the main site of BRI1 signaling activity, the very first steps of signal transmission are still elusive. Recently, it was shown that the initiation of BR signal transduction requires the interaction of BRI1 with its SOMATIC EMBRYOGENESIS RECEPTOR-LIKE KINASE (SERK) coreceptors. In addition, the resolved structure of the BRI1 ectodomain suggested that BRI1-ASSOCIATED KINASE1 [BAK1](SERK3) may constitute a component of the ligand-perceiving receptor complex. Therefore, we investigated the spatial correlation between BRI1 and BAK1(SERK3) in the natural habitat of both leucine-rich repeat receptor-like kinases using comparative colocalization analysis and fluorescence lifetime imaging microscopy. We show that activation of BR signaling by exogenous ligand application resulted in both elevated colocalization between BRI1 and BAK1(SERK3) and an about 50% increase of receptor heterooligomerization in the PM of live Arabidopsis root epidermal cells. However, large populations of BRI1 and BAK1(SERK3) colocalized independently of BRs. Moreover, we could visualize that approximately 7% of the BRI1 PM pool constitutively heterooligomerizes with BAK1(SERK3) in live root cells. We propose that only small populations of PM-located BRI1 and BAK1(SERK3) receptors participate in active BR signaling and that the initiation of downstream signal transduction involves preassembled BRI1-BAK1(SERK3) heterooligomers