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  • Biodiversitätsforschung  (4)
  • 1
    In: Plant Physiology, Oxford University Press (OUP), Vol. 191, No. 1 ( 2023-01-02), p. 265-279
    Kurzfassung: Cell cycle progression and the phytohormones auxin and abscisic acid (ABA) play key roles in primary root growth, but how ABA mediates the transcription of cell cycle-related genes and the mechanism of crosstalk between ABA and auxin requires further research. Here, we report that ABA inhibits primary root growth by regulating the ABA INSENSITIVE4 (ABI4)-CYCLIN-DEPENDENT KINASE B2;2 (CDKB2;2)/CYCLIN B1;1 (CYCB1;1) module-mediated cell cycle as well as auxin biosynthesis in Arabidopsis (Arabidopsis thaliana). ABA induced ABI4 transcription in the primary root tip, and the abi4 mutant showed an ABA-insensitive phenotype in primary root growth. Compared with the wild type (WT), the meristem size and cell number of the primary root in abi4 increased in response to ABA. Further, the transcription levels of several cell-cycle positive regulator genes, including CDKB2;2 and CYCB1;1, were upregulated in abi4 primary root tips. Subsequent chromatin immunoprecipitation (ChIP)-seq, ChIP-qPCR, and biochemical analysis revealed that ABI4 repressed the expression of CDKB2;2 and CYCB1;1 by physically interacting with their promoters. Genetic analysis demonstrated that overexpression of CDKB2;2 or CYCB1;1 fully rescued the shorter primary root phenotype of ABI4-overexpression lines, and consistently, abi4/cdkb2;2-cr or abi4/cycb1;1-cr double mutations largely rescued the ABA-insensitive phenotype of abi4 with regard to primary root growth. The expression levels of DR5promoter-GFP and PIN1promoter::PIN1-GFP in abi4 primary root tips were significantly higher than those in WT after ABA treatment, with these changes being consistent with changes in auxin concentration and expression patterns of auxin biosynthesis genes. Taken together, these findings indicated that ABA inhibits primary root growth through ABI4-mediated cell cycle and auxin-related regulatory pathways.
    Materialart: Online-Ressource
    ISSN: 0032-0889 , 1532-2548
    RVK:
    Sprache: Englisch
    Verlag: Oxford University Press (OUP)
    Publikationsdatum: 2023
    ZDB Id: 2004346-6
    ZDB Id: 208914-2
    SSG: 12
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 2
    Online-Ressource
    Online-Ressource
    Proceedings of the National Academy of Sciences ; 2016
    In:  Proceedings of the National Academy of Sciences Vol. 113, No. 13 ( 2016-03-29)
    In: Proceedings of the National Academy of Sciences, Proceedings of the National Academy of Sciences, Vol. 113, No. 13 ( 2016-03-29)
    Kurzfassung: The extracellular domain of the (pro)renin receptor (PRR) is cleaved to produce a soluble (pro)renin receptor (sPRR) that is detected in biological fluid and elevated under certain pathological conditions. The present study was performed to define the antidiuretic action of sPRR and its potential interaction with liver X receptors (LXRs), which are known regulators of urine-concentrating capability. Water deprivation consistently elevated urinary sPRR excretion in mice and humans. A template-based algorithm for protein–protein interaction predicted the interaction between sPRR and frizzled-8 (FZD8), which subsequently was confirmed by coimmunoprecipitation. A recombinant histidine-tagged sPRR (sPRR-His) in the nanomolar range induced a remarkable increase in the abundance of renal aquaporin 2 (AQP2) protein in primary rat inner medullary collecting duct cells. The AQP2 up-regulation relied on sequential activation of FZD8-dependent β-catenin signaling and cAMP–PKA pathways. Inhibition of FZD8 or tankyrase in rats induced polyuria, polydipsia, and hyperosmotic urine. Administration of sPRR-His alleviated the symptoms of diabetes insipidus induced in mice by vasopressin 2 receptor antagonism. Administration of the LXR agonist TO901317 to C57/BL6 mice induced polyuria and suppressed renal AQP2 expression associated with reduced renal PRR expression and urinary sPRR excretion. Administration of sPRR-His reversed most of the effects of TO901317. In cultured collecting duct cells, TO901317 suppressed PRR protein expression, sPRR release, and PRR transcriptional activity. Overall we demonstrate, for the first time to our knowledge, that sPRR exerts antidiuretic action via FZD8-dependent stimulation of AQP2 expression and that inhibition of this pathway contributes to the pathogenesis of diabetes insipidus induced by LXR agonism.
    Materialart: Online-Ressource
    ISSN: 0027-8424 , 1091-6490
    RVK:
    RVK:
    Sprache: Englisch
    Verlag: Proceedings of the National Academy of Sciences
    Publikationsdatum: 2016
    ZDB Id: 209104-5
    ZDB Id: 1461794-8
    SSG: 11
    SSG: 12
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 3
    Online-Ressource
    Online-Ressource
    Oxford University Press (OUP) ; 2020
    In:  Journal of Molecular Cell Biology Vol. 12, No. 4 ( 2020-05-18), p. 322-325
    In: Journal of Molecular Cell Biology, Oxford University Press (OUP), Vol. 12, No. 4 ( 2020-05-18), p. 322-325
    Materialart: Online-Ressource
    ISSN: 1759-4685
    Sprache: Englisch
    Verlag: Oxford University Press (OUP)
    Publikationsdatum: 2020
    ZDB Id: 2500949-7
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 4
    Online-Ressource
    Online-Ressource
    Proceedings of the National Academy of Sciences ; 2020
    In:  Proceedings of the National Academy of Sciences Vol. 117, No. 38 ( 2020-09-22), p. 23869-23878
    In: Proceedings of the National Academy of Sciences, Proceedings of the National Academy of Sciences, Vol. 117, No. 38 ( 2020-09-22), p. 23869-23878
    Kurzfassung: Mounting evidence has associated Zika virus (ZIKV) infection with congenital malformations, including microcephaly, which raises global alarm. Nonetheless, mechanisms by which ZIKV disrupts neurogenesis and causes microcephaly are far from being understood. In this study, we discovered direct effects of ZIKV on neural progenitor cell development by inducing caspase-1– and gasdermin D (GSDMD)-mediated pyroptotic cell death, linking ZIKV infection with the development of microcephaly. Importantly, caspase-1 depletion or its inhibitor VX-765 treatment reduced ZIKV-induced inflammatory responses and pyroptosis, and substantially attenuated neuropathology and brain atrophy in vivo. Collectively, our data identify caspase-1– and GSDMD-mediated pyroptosis in neural progenitor cells as a previously unrecognized mechanism for ZIKV-related pathological effects during neural development, and also provide treatment options for ZIKV-associated diseases.
    Materialart: Online-Ressource
    ISSN: 0027-8424 , 1091-6490
    RVK:
    RVK:
    Sprache: Englisch
    Verlag: Proceedings of the National Academy of Sciences
    Publikationsdatum: 2020
    ZDB Id: 209104-5
    ZDB Id: 1461794-8
    SSG: 11
    SSG: 12
    Standort Signatur Einschränkungen Verfügbarkeit
    BibTip Andere fanden auch interessant ...
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