| 1. |
- Yu, Guimei, et al.
(författare)
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Structure of Arabidopsis SOQ1 lumenal region unveils C-terminal domain essential for negative regulation of photoprotective qH
- 2022
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Ingår i: Nature Plants. - : Nature Publishing Group. - 2055-0278. ; 8:7, s. 840-855
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Tidskriftsartikel (refereegranskat)abstract
- Non-photochemical quenching (NPQ) plays an important role for phototrophs in decreasing photo-oxidative damage. qH is a sustained form of NPQ and depends on the plastid lipocalin (LCNP). A thylakoid membrane-anchored protein SUPPRESSOR OF QUENCHING1 (SOQ1) prevents qH formation by inhibiting LCNP. SOQ1 suppresses qH with its lumen-located thioredoxin (Trx)-like and NHL domains. Here we report structural data, genetic modification and biochemical characterization of Arabidopsis SOQ1 lumenal domains. Our results show that the Trx-like and NHL domains are associated together, with the cysteine motif located at their interface. Residue E859, required for SOQ1 function, is pivotal for maintaining the Trx–NHL association. Importantly, the C-terminal region of SOQ1 forms an independent β-stranded domain that has structural homology to the N-terminal domain of bacterial disulfide bond protein D and is essential for negative regulation of qH. Furthermore, SOQ1 is susceptible to cleavage at the loops connecting the neighbouring lumenal domains both in vitro and in vivo, which could be a regulatory process for its suppression function of qH.
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| 2. |
- Yu, Guimei, et al.
(författare)
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Structure of SOQ1 lumenal domains identifies potential disulfide exchange for negative regulation of photoprotection, qH
- 2024
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Annan publikation (övrigt vetenskapligt/konstnärligt)abstract
- Non-photochemical quenching (NPQ) plays an important role for phototrophs in decreasing photo-oxidative damage. qH is a sustained component of NPQ and depends on the plastid lipocalin (LCNP). A thylakoid membrane-anchored protein SUPPRESSOR OF QUENCHING1 (SOQ1) prevents qH formation by inhibiting LCNP. SOQ1 suppresses qH with its lumen-located C-terminal Trx-like and NHL domains. Here we report crystal structures and biochemical characterization of SOQ1 lumenal domains. Our results show that the Trx-like and NHL domains are stably associated, with the potential redox-active motif located at their interface. Residue E859 essential for SOQ1 function is pivotal for mediating the inter-domain interaction. Moreover, the C-terminal region of SOQ1 forms an independent β-stranded domain, which possibly interacts with the Trx-like domain through disulfide exchange. Furthermore, SOQ1 is susceptible to cleavage at the loops connecting the neighboring domains both in vitro and in vivo, which could be a regulatory process for its suppression function of qH.
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| 3. |
- Jang, Seon-Kyeong, et al.
(författare)
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Rare genetic variants explain missing heritability in smoking.
- 2022
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Ingår i: Nature human behaviour. - : Springer Science and Business Media LLC. - 2397-3374. ; 6:11, s. 1577-1586
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Tidskriftsartikel (refereegranskat)abstract
- Common genetic variants explain less variation in complex phenotypes than inferred from family-based studies, and there is a debate on the source of this 'missing heritability'. We investigated the contribution of rare genetic variants to tobacco use with whole-genome sequences from up to 26,257 unrelated individuals of European ancestries and 11,743 individuals of African ancestries. Across four smoking traits, single-nucleotide-polymorphism-based heritability ([Formula: see text]) was estimated from 0.13 to 0.28 (s.e., 0.10-0.13) in European ancestries, with 35-74% of it attributable to rare variants with minor allele frequencies between 0.01% and 1%. These heritability estimates are 1.5-4 times higher than past estimates based on common variants alone and accounted for 60% to 100% of our pedigree-based estimates of narrow-sense heritability ([Formula: see text], 0.18-0.34). In the African ancestry samples, [Formula: see text] was estimated from 0.03 to 0.33 (s.e., 0.09-0.14) across the four smoking traits. These results suggest that rare variants are important contributors to the heritability of smoking.
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| 4. |
- Liu, Rui, et al.
(författare)
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How should water resources be allocated for shale gas development? : An exploratory study in China
- 2022
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Ingår i: Sustainable Production and Consumption. - : Elsevier. - 2352-5509. ; 30, s. 1001-1018
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Tidskriftsartikel (refereegranskat)abstract
- Water scarcity has emerged as one of the most important global challenges of the twenty-first century. With rising demand for energy, and water being a critical input in energy production, the availability of water resources has put energy sustainable production under growing strain. While unconventional natural gas (especially shale gas) is seen as an important bridge for promoting the transition of energy system from high to low carbon, water availability is a significant constraint on the development of energy resources owing to the massive quantity of water used by the hydraulic fracturing. Against this background, our study aims to optimize the allocation of regionally scarce water resources for fostering integrated economic, social, and environmental growth in shale gas development plays. In light of the uncertainty inherent in the water supply management system for shale gas development, this work employed the Interval Two-stage Stochastic Programming (ITSP) to establish an optimal allocation model for water resources between wells jointly dispatched by surface water, underground water and reused water. The model predicted water scarcity, optimal water allocation, and the total benefit of the shale gas development water supply system under various scenarios. Furthermore, when compared to the Twostage Stochastic Programming (TSP) model results, it was found that the ITSP model's interval value may present decision makers with more ideas and options than the TSP model. In addition, since the ITSP model is oblivious to the system risk issue, it incorporated robust optimization into the original ITSP model to build the Interval Two-stage Robust Stochastic Programming (ITRSP) model. Our findings were expressed as intervals that more accurately represent the actual optimal allocation of water resources, which also provided a broader decision-making space for decision makers in managing shale gas development water supply management schemes. (c) 2022 Institution of Chemical Engineers. Published by Elsevier Ltd. All rights reserved.
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| 5. |
- Weinstock, Joshua S, et al.
(författare)
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Aberrant activation of TCL1A promotes stem cell expansion in clonal haematopoiesis.
- 2023
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Ingår i: Nature. - 1476-4687. ; 616:7958, s. 755-763
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Tidskriftsartikel (refereegranskat)abstract
- Mutations in a diverse set of driver genes increase the fitness of haematopoietic stem cells (HSCs), leading to clonal haematopoiesis1. These lesions are precursors for blood cancers2-6, but the basis of their fitness advantage remains largely unknown, partly owing to a paucity of large cohorts in which the clonal expansion rate has been assessed by longitudinal sampling. Here, to circumvent this limitation, we developed a method to infer the expansion rate from data from a single time point. We applied this method to 5,071 people with clonal haematopoiesis. A genome-wide association study revealed that a common inherited polymorphism in the TCL1A promoter was associated with a slower expansion rate in clonal haematopoiesis overall, but the effect varied by driver gene. Those carrying this protective allele exhibited markedly reduced growth rates or prevalence of clones with driver mutations in TET2, ASXL1, SF3B1 and SRSF2, butthis effect was not seen inclones withdriver mutations in DNMT3A. TCL1A was not expressed in normal or DNMT3A-mutated HSCs, but the introduction of mutations in TET2 or ASXL1 led to the expression of TCL1A protein and the expansion of HSCs in vitro. The protective allele restricted TCL1A expression and expansion of mutant HSCs, as did experimentalknockdown of TCL1A expression. Forced expression of TCL1A promoted the expansion of human HSCs in vitro and mouse HSCs in vivo. Our results indicate that the fitness advantage of several commonly mutated driver genes in clonal haematopoiesis may be mediated by TCL1A activation.
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