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  • 1
    Online Resource
    Online Resource
    The Amborella Genome and the Evolution of Flowering Plants
    American Association for the Advancement of Science (AAAS) ; 2013
    In:  Science Vol. 342, No. 6165 ( 2013-12-20)
    Details
    In: Science, American Association for the Advancement of Science (AAAS), Vol. 342, No. 6165 ( 2013-12-20)
    Abstract: Amborella trichopoda is strongly supported as the single living species of the sister lineage to all other extant flowering plants, providing a unique reference for inferring the genome content and structure of the most recent common ancestor (MRCA) of living angiosperms. Sequencing the Amborella genome, we identified an ancient genome duplication predating angiosperm diversification, without evidence of subsequent, lineage-specific genome duplications. Comparisons between Amborella and other angiosperms facilitated reconstruction of the ancestral angiosperm gene content and gene order in the MRCA of core eudicots. We identify new gene families, gene duplications, and floral protein-protein interactions that first appeared in the ancestral angiosperm. Transposable elements in Amborella are ancient and highly divergent, with no recent transposon radiations. Population genomic analysis across Amborella ’s native range in New Caledonia reveals a recent genetic bottleneck and geographic structure with conservation implications.
    Type of Medium: Online Resource
    ISSN: 0036-8075 , 1095-9203
    URL: Article
    DOI: 10.1126/science.1241089
    RVK:
    TA 1000
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    WA 15000
    Language: English
    Publisher: American Association for the Advancement of Science (AAAS)
    Publication Date: 2013
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  • 2
    Online Resource
    Online Resource
    Bmi1 regulates mitochondrial function and the DNA damage response pathway
    Springer Science and Business Media LLC ; 2009
    In:  Nature Vol. 459, No. 7245 ( 2009-5), p. 387-392
    Details
    In: Nature, Springer Science and Business Media LLC, Vol. 459, No. 7245 ( 2009-5), p. 387-392
    Type of Medium: Online Resource
    ISSN: 0028-0836 , 1476-4687
    URL: Article
    DOI: 10.1038/nature08040
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    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2009
    detail.hit.zdb_id: 120714-3
    detail.hit.zdb_id: 1413423-8
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  • 3
    Online Resource
    Online Resource
    Acetylcholine ameliorates colitis by promoting IL-10 secretion of monocytic myeloid-derived suppressor cells through the nAChR/ERK pathway
    Proceedings of the National Academy of Sciences ; 2021
    In:  Proceedings of the National Academy of Sciences Vol. 118, No. 11 ( 2021-03-16)
    Details
    In: Proceedings of the National Academy of Sciences, Proceedings of the National Academy of Sciences, Vol. 118, No. 11 ( 2021-03-16)
    Abstract: The alteration of the enteric nervous system (ENS) and its role in neuroimmune modulation remain obscure in the pathogenesis of inflammatory bowel diseases (IBDs). Here, by using the xCell tool and the latest immunolabeling-enabled three-dimensional (3D) imaging of solvent-cleared organs technique, we found severe pathological damage of the entire ENS and decreased expression of choline acetyltransferase (ChAT) in IBD patients. As a result, acetylcholine (ACh), a major neurotransmitter of the nervous system synthesized by ChAT, was greatly reduced in colon tissues of both IBD patients and colitis mice. Importantly, administration of ACh via enema remarkably ameliorated colitis, which was proved to be directly dependent on monocytic myeloid-derived suppressor cells (M-MDSCs). Furthermore, ACh was demonstrated to promote interleukin-10 secretion of M-MDSCs and suppress the inflammation through activating the nAChR/ERK pathway. The present data reveal that the cholinergic signaling pathway in the ENS is impaired during colitis and uncover an ACh-MDSCs neuroimmune regulatory pathway, which may offer promising therapeutic strategies for IBDs.
    Type of Medium: Online Resource
    ISSN: 0027-8424 , 1091-6490
    URL: Article
    DOI: 10.1073/pnas.2017762118
    RVK:
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    Language: English
    Publisher: Proceedings of the National Academy of Sciences
    Publication Date: 2021
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  • 4
    Online Resource
    Online Resource
    Reducing brassinosteroid signalling enhances grain yield in semi-dwarf wheat
    Springer Science and Business Media LLC ; 2023
    In:  Nature Vol. 617, No. 7959 ( 2023-05-04), p. 118-124
    Details
    In: Nature, Springer Science and Business Media LLC, Vol. 617, No. 7959 ( 2023-05-04), p. 118-124
    Abstract: Modern green revolution varieties of wheat ( Triticum aestivum L.) confer semi-dwarf and lodging-resistant plant architecture owing to the Reduced height-B1b ( Rht-B1b ) and Rht-D1b alleles 1 . However, both Rht-B1b and Rht-D1b are gain-of-function mutant alleles encoding gibberellin signalling repressors that stably repress plant growth and negatively affect nitrogen-use efficiency and grain filling 2–5 . Therefore, the green revolution varieties of wheat harbouring Rht-B1b or Rht-D1b usually produce smaller grain and require higher nitrogen fertilizer inputs to maintain their grain yields. Here we describe a strategy to design semi-dwarf wheat varieties without the need for Rht-B1b or Rht-D1b alleles. We discovered that absence of Rht-B1 and ZnF-B (encoding a RING-type E3 ligase) through a natural deletion of a haploblock of about 500 kilobases shaped semi-dwarf plants with more compact plant architecture and substantially improved grain yield (up to 15.2%) in field trials. Further genetic analysis confirmed that the deletion of ZnF-B induced the semi-dwarf trait in the absence of the Rht-B1b and Rht-D1b alleles through attenuating brassinosteroid (BR) perception. ZnF acts as a BR signalling activator to facilitate proteasomal destruction of the BR signalling repressor BRI1 kinase inhibitor 1 (TaBKI1), and loss of ZnF stabilizes TaBKI1 to block BR signalling transduction. Our findings not only identified a pivotal BR signalling modulator but also provided a creative strategy to design high-yield semi-dwarf wheat varieties by manipulating the BR signal pathway to sustain wheat production.
    Type of Medium: Online Resource
    ISSN: 0028-0836 , 1476-4687
    URL: Article
    DOI: 10.1038/s41586-023-06023-6
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    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2023
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    detail.hit.zdb_id: 1413423-8
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  • 5
    Online Resource
    Online Resource
    Bright Infrared Emission from Electrically Induced Excitons in Carbon Nanotubes
    American Association for the Advancement of Science (AAAS) ; 2005
    In:  Science Vol. 310, No. 5751 ( 2005-11-18), p. 1171-1174
    Details
    In: Science, American Association for the Advancement of Science (AAAS), Vol. 310, No. 5751 ( 2005-11-18), p. 1171-1174
    Abstract: We used the high local electric fields at the junction between the suspended and supported parts of a single carbon nanotube molecule to produce unusually bright infrared emission under unipolar operation. Carriers were accelerated by band-bending at the suspension interface, and they created excitons that radiatively recombined. This excitation mechanism is ∼1000 times more efficient than recombination of independently injected electrons and holes, and it results from weak electron-phonon scattering and strong electron-hole binding caused by one-dimensional confinement. The ensuing high excitation density allows us to observe emission from higher excited states not seen by photoexcitation. The excitation mechanism of these states was analyzed.
    Type of Medium: Online Resource
    ISSN: 0036-8075 , 1095-9203
    URL: Article
    DOI: 10.1126/science.1119177
    RVK:
    TA 1000
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    WA 15000
    Language: English
    Publisher: American Association for the Advancement of Science (AAAS)
    Publication Date: 2005
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  • 6
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    Online Resource
    Alternative Gnas gene products have opposite effects on glucose and lipid metabolism
    Proceedings of the National Academy of Sciences ; 2005
    In:  Proceedings of the National Academy of Sciences Vol. 102, No. 20 ( 2005-05-17), p. 7386-7391
    Details
    In: Proceedings of the National Academy of Sciences, Proceedings of the National Academy of Sciences, Vol. 102, No. 20 ( 2005-05-17), p. 7386-7391
    Abstract: Gnas is an imprinted gene with multiple gene products resulting from alternative splicing of different first exons onto a common exon 2. These products include stimulatory G protein α-subunit (G s α), the G protein required for receptor-stimulated cAMP production; extralarge G s α (XLαs), a paternally expressed G s α isoform; and neuroendocrine-specific protein (NESP55), a maternally expressed chromogranin-like protein. G s α undergoes tissue-specific imprinting, being expressed primarily from the maternal allele in certain tissues. Heterozygous mutation of exon 2 on the maternal (E2 m-/+ ) or paternal (E2 +/p- ) allele results in opposite effects on energy metabolism. E2 m-/+ mice are obese and hypometabolic, whereas E2 +/p- mice are lean and hypermetabolic. We now studied the effects of G s α deficiency without disrupting other Gnas gene products by deleting G s α exon 1 (E1). E1 +/p- mice lacked the E2 +/p- phenotype and developed obesity and insulin resistance. The lean, hypermetabolic, and insulin-sensitive E2 +/p- phenotype appears to result from XLαs deficiency, whereas loss of paternal-specific G s α expression in E1 +/p- mice leads to an opposite metabolic phenotype. Thus, alternative Gnas gene products have opposing effects on glucose and lipid metabolism. Like E2 m-/+ mice, E1 m-/+ mice had s.c. edema at birth, presumably due to loss of maternal G s α expression. However, E1 m-/+ mice differed from E2 m-/+ mice in other respects, raising the possibility for the presence of other maternal-specific gene products. E1 m-/+ mice had more severe obesity and insulin resistance and lower metabolic rate relative to E1 +/p- mice. Differences between E1 m-/+ and E1 +/p- mice presumably result from differential effects on G s α expression in tissues where G s α is normally imprinted.
    Type of Medium: Online Resource
    ISSN: 0027-8424 , 1091-6490
    URL: Article
    DOI: 10.1073/pnas.0408268102
    RVK:
    TA 1000
    RVK:
    WA 15000
    Language: English
    Publisher: Proceedings of the National Academy of Sciences
    Publication Date: 2005
    detail.hit.zdb_id: 209104-5
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  • 7
    Online Resource
    Online Resource
    Identification of the control region for tissue-specific imprinting of the stimulatory G protein α-subunit
    Proceedings of the National Academy of Sciences ; 2005
    In:  Proceedings of the National Academy of Sciences Vol. 102, No. 15 ( 2005-04-12), p. 5513-5518
    Details
    In: Proceedings of the National Academy of Sciences, Proceedings of the National Academy of Sciences, Vol. 102, No. 15 ( 2005-04-12), p. 5513-5518
    Abstract: Gnas is a complex gene with multiple imprinted promoters. The upstream Nesp and Nespas / Gnasxl promoters are paternally and maternally methylated, respectively. The downstream promoter for the stimulatory G protein α-subunit (G s α) is unmethylated, although in some tissues (e.g., renal proximal tubules), G s α is poorly expressed from the paternal allele. Just upstream of the G s α promoter is a primary imprint mark (1A region) where maternal-specific methylation is established during oogenesis. Pseudohypoparathyroidism type 1B, a disorder of renal parathyroid hormone resistance, is associated with loss of 1A methylation. Analysis of embryos of Dnmt3L –/– mothers (which cannot methylate maternal imprint marks) showed that Nesp , Nespas / Gnasxl , and 1A imprinting depend on one or more maternal primary imprint marks. We generated mice with deletion of the 1A differentially methylated region. These mice had normal Nesp-Nespas / Gnasxl imprinting, indicating that the Gnas locus contains two independent imprinting domains ( Nespas-Nespas / Gnasxl and 1A-G s α) controlled by distinct maternal primary imprint marks. Paternal, but not maternal, 1A deletion resulted in G s α overexpression in proximal tubules and evidence for increased parathyroid hormone sensitivity but had no effect on G s α expression in other tissues where G s α is normally not imprinted. The 1A region is a maternal imprint mark that contains one or more methylation-sensitive cis-acting elements that suppress G s α expression from the paternal allele in a tissue-specific manner.
    Type of Medium: Online Resource
    ISSN: 0027-8424 , 1091-6490
    URL: Article
    DOI: 10.1073/pnas.0408262102
    RVK:
    TA 1000
    RVK:
    WA 15000
    Language: English
    Publisher: Proceedings of the National Academy of Sciences
    Publication Date: 2005
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    detail.hit.zdb_id: 1461794-8
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  • 8
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    Sustained ER stress promotes hyperglycemia by increasing glucagon action through the deubiquitinating enzyme USP14
    Proceedings of the National Academy of Sciences ; 2019
    In:  Proceedings of the National Academy of Sciences Vol. 116, No. 43 ( 2019-10-22), p. 21732-21738
    Details
    In: Proceedings of the National Academy of Sciences, Proceedings of the National Academy of Sciences, Vol. 116, No. 43 ( 2019-10-22), p. 21732-21738
    Abstract: Endoplasmic reticulum (ER) stress plays an important role in metabolic diseases like obesity and type 2 diabetes mellitus (T2DM), although the underlying mechanisms and regulatory pathways remain to be elucidated. Here, we induced chronic low-grade ER stress in lean mice to levels similar to those in high-fat diet (HFD)–fed obese mice and found that it promoted hyperglycemia due to enhanced hepatic gluconeogenesis. Mechanistically, sustained ER stress up-regulated the deubiquitinating enzyme ubiquitin-specific peptidase 14 (USP14), which increased the stability and levels of 3′,5′-cyclic monophosphate–responsive element binding (CREB) protein (CBP) to enhance glucagon action and hepatic gluconeogenesis. Exogenous overexpression of USP14 in the liver significantly increased hepatic glucose output. Consistent with this, liver-specific knockdown of USP14 abrogated the effects of ER stress on glucose metabolism, and also improved hyperglycemia and glucose intolerance in obese mice. In conclusion, our findings show a mechanism underlying ER stress-induced disruption of glucose homeostasis, and present USP14 as a potential therapeutic target against T2DM.
    Type of Medium: Online Resource
    ISSN: 0027-8424 , 1091-6490
    URL: Article
    DOI: 10.1073/pnas.1907288116
    RVK:
    TA 1000
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    WA 15000
    Language: English
    Publisher: Proceedings of the National Academy of Sciences
    Publication Date: 2019
    detail.hit.zdb_id: 209104-5
    detail.hit.zdb_id: 1461794-8
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  • 9
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    Online Resource
    Augmented Wnt Signaling in a Mammalian Model of Accelerated Aging
    American Association for the Advancement of Science (AAAS) ; 2007
    In:  Science Vol. 317, No. 5839 ( 2007-08-10), p. 803-806
    Details
    In: Science, American Association for the Advancement of Science (AAAS), Vol. 317, No. 5839 ( 2007-08-10), p. 803-806
    Abstract: The contribution of stem and progenitor cell dysfunction and depletion in normal aging remains incompletely understood. We explored this concept in the Klotho mouse model of accelerated aging. Analysis of various tissues and organs from young Klotho mice revealed a decrease in stem cell number and an increase in progenitor cell senescence. Because klotho is a secreted protein, we postulated that klotho might interact with other soluble mediators of stem cells. We found that klotho bound to various Wnt family members. In a cell culture model, the Wnt-klotho interaction resulted in the suppression of Wnt biological activity. Tissues and organs from klotho-deficient animals showed evidence of increased Wnt signaling, and ectopic expression of klotho antagonized the activity of endogenous and exogenous Wnt. Both in vitro and in vivo, continuous Wnt exposure triggered accelerated cellular senescence. Thus, klotho appears to be a secreted Wnt antagonist and Wnt proteins have an unexpected role in mammalian aging.
    Type of Medium: Online Resource
    ISSN: 0036-8075 , 1095-9203
    URL: Article
    DOI: 10.1126/science.1143578
    RVK:
    TA 1000
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    Language: English
    Publisher: American Association for the Advancement of Science (AAAS)
    Publication Date: 2007
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  • 10
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    Resveratrol and polydatin as modulators of Ca 2+ mobilization in the cardiovascular system
    Wiley ; 2017
    In:  Annals of the New York Academy of Sciences Vol. 1403, No. 1 ( 2017-09), p. 82-91
    Details
    In: Annals of the New York Academy of Sciences, Wiley, Vol. 1403, No. 1 ( 2017-09), p. 82-91
    Abstract: In the cardiovascular system, Ca 2+ controls cardiac excitation–contraction coupling and vascular contraction and dilation. Disturbances in intracellular Ca 2+ homeostasis induce malfunctions of the cardiovascular system, including cardiac pump dysfunction, arrhythmia, remodeling, and apoptosis, as well as hypertension and impairment of vascular reactivity. Therefore, developing drugs and strategies manipulating Ca 2+ handling are highly valued in the treatment of cardiovascular disease. Resveratrol (Res) and polydatin (PD), a Res glucoside, have been well established to have beneficial effects on improving cardiovascular function. Studies from our laboratory and others have demonstrated that they exhibit inotropic effects on normal heart and therapeutic effects on hypertension, cardiac ischemia/reperfusion injury, hypertrophy, and heart failure by manipulating Ca 2+ mobilization. The actions of Res and PD on Ca 2+ signals delicately manipulated by multiple Ca 2+ ‐handling proteins are pleiotropic and somewhat controversial, depending on cellular species and intracellular oxidative status. Here, we focus on the effects of Res and PD on controlling Ca 2+ homeostasis in the heart and vasculature under normal and diseased conditions and highlight the key direct and indirect molecules mediating these effects.
    Type of Medium: Online Resource
    ISSN: 0077-8923 , 1749-6632
    URL: Issue
    URL: Article
    DOI: 10.1111/nyas.2017.1403.issue-1
    DOI: 10.1111/nyas.13386
    RVK:
    TD 7650
    Language: English
    Publisher: Wiley
    Publication Date: 2017
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    detail.hit.zdb_id: 211003-9
    detail.hit.zdb_id: 2071584-5
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