Human ABI3 peptide

To conserve water plants close the stomata in response to increased abscisic acid (ABA) content. Previous studies have shown that plants developed in high relative air humidity (RH >85%) develop malfunctioning stomata and have lower ABA content. It has therefore been hypothesized that low ABA content during development results in malfunctioning stomata. In this study the stomatal functioning of Arabidopsis thaliana was evaluated and the content, biosynthesis and catabolism of ABA were quantified. It was found that even though they have lower ABA content during growth, plants developed under high RH were able to produce large amounts of ABA in detached leaves, but still had high water loss. Plants developed in high RH had increased ABA 8'-hydroxylase activity of cytochrome P450CYP707A. Also, plants developed in high RH that were sprayed with ABA or Abscinazole-E1, which inhibits the ABA 8'-hydroxylase activity, had reduced stomatal apertures. ABA deficient mutants had higher water loss in detached leaves than wild type plants in both high and moderate RH. From these results we therefore conclude that continuous low ABA content in high RH is due to increased ABA catabolism by the ABA 8'-hydroxylase activity of cytochrome P450CYP707A. The continuous low ABA content result in reduced ability to close the stomata. (C) 2015 Elsevier B.V. All rights reserved.

Missense variantsABI3_rs616338-T andPLCG2_rs72824905-G were previously associated with elevated or reduced risk of Alzheimer's disease (AD), respectively. Despite reports of associations with other neurodegenerative diseases, there are few studies of these variants in purely neuropathologically diagnosed cohorts. Further, the effect of these mutations on neurodegenerative disease pathologies is unknown. In this study, we tested the effects ofABI3_rs616338-T andPLCG2_rs72824905-G on disease risk in autopsy cohorts comprised of 973 patients diagnosed neuropathologically with Lewy body disease (LBD-NP) and 1040 with progressive supranuclear palsy (PSP), compared to 3351 controls. LBD-NP patients were further categorized as high, intermediate and low likelihood of clinical dementia with Lewy bodies (DLB-CL) based on DLB Consortium criteria. We also tested for association with both Braak neurofibrillary tau tangle (n(Total) = 2008, n(PSP) = 1037, n(LBD-NP) = 971) and Thal phase amyloid plaque scores (n(Total) = 1786, n(PSP) = 1018, n(LBD-NP) = 768). Additionally, 841 PSP patients had quantitative tau neuropathology measures that were assessed for genetic associations. There was no statistically significant association with disease risk for either LBD-NP or PSP in our study. LBD intermediate category disease risk was significantly associated withABI3_rs616338-T (OR = 2.65, 95% CI 1.46-4.83,p = 0.001).PLCG2_rs72824905-G was associated with lower Braak stage (ss = - 0.822, 95% CI - 1.439 to - 0.204,p = 0.009). This effect was more pronounced in the PSP (ss = - 0.995, 95% CI - 1.773 to - 0.218,p = 0.012) than LBD-NP patients (ss = - 0.292, 95% CI - 1.283 to 0.698,p = 0.563).PLCG2_rs72824905-G also showed association with reduced quantitative tau pathology for each lesion type and overall tau burden in PSP (ss = - 0.638, 95% CI - 1.139 to - 0.136,p = 0.013). These findings support a role forPLCG2_rs72824905-G in suppressing tau neuropathology.ABI3_rs616338-T may influence disease risk specifically in the LBD-NP intermediate category comprised of patients with diffuse neocortical or limbic LB, concurrently with moderate or high AD neuropathology, respectively. Our study provides a potential mechanism of action for the missensePLCG2variant and suggests a differential disease risk effect forABI3in a distinct LBD-NP neuropathologic category.