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Botryosphaeria dieback (BD) is a worldwide grapevine trunk disease constituting a serious threat for sustainable grapevine production, especially in the context of climate change. Effective treatments to control BD are still lacking, prompting the exploration of new non-chemical alternatives. Among these, BioControl Agents (BCAs), such as spp. and spp., described as promising. This study aims to thoroughly investigate the physiological changes in grapevines induced by two BCAs, ( PTA-271) and ( SC1), which are used to protect two cultivars from Bt67 (Np-Bt67) infection. Using non-target transcriptomic analysis (RNA-seq) and validation by qRT-PCR, this research offers novel insights into the molecular responses associated to Np-Bt67 infection in Chardonnay and Tempranillo cultivars, in relationship with the protective mechanisms conferred by each BCA. RNA-seq reveals that cultivars show no common transcriptional changes upon pathogen challenge. In Chardonnay, changes are mainly related to terpene/carotenoid pathways, while in Tempranillo, they mostly relate to amino acid transport and photosynthesis. Following the inoculation of protective BCA, changes are also distinct between infected cultivars: PTA-271 protecting effect against infected Chardonnay is mainly related to the phenylpropanoid pathway and secondary metabolic processes, whereas that of SC1 for Tempranillo correlates with much more metabolic changes. Consecutive validation by qRT-PCR provides markers indicating grapevine susceptibility vs. protection against Np-Bt67, some of which are shared by both cultivars. These markers could offer valuable tools for monitoring the health status of grapevine towards .
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http://dx.doi.org/10.1094/PHYTO-12-24-0399-R | DOI Listing |
Biosci Biotechnol Biochem
September 2025
College of Life Sciences, Ritsumeikan University, 1-1-1 Nojihigashi, Kusatsu, Shiga 525-8577, Japan.
Selenium is an essential trace element in many organisms but becomes toxic at elevated concentrations. At moderately increased, non-lethal levels, selenite triggers both selenium utilization and stress responses in microorganisms. However, the thresholds of such responses in archaea remain poorly understood.
View Article and Find Full Text PDFJ Gerontol A Biol Sci Med Sci
September 2025
Department of Physical Medicine and Rehabilitation, Harvard Medical School, Boston, USA.
Maintenance of organismal function requires tightly regulated biomolecular communication. However, with aging, communication deteriorates, thereby disrupting effective information flow. Using information theory applied to skeletal muscle single cell RNA-seq data from young, middle-aged, and aged animals, we quantified the loss of communication efficiency over time.
View Article and Find Full Text PDFElife
September 2025
State Key Laboratory of Oncology in South China, Guangdong Provincial Clinical Research Center for Cancer, Sun Yat-sen University Cancer Center, Guangzhou, China.
Innate immune cells can acquire a memory phenotype, termed trained immunity, but the mechanism underlying the regulation of trained immunity remains largely elusive. Here, we demonstrate that inhibition of Aurora kinase A (AurA) dampens trained immunity induced by β-glucan. ATAC-seq and RNA-seq analysis reveal that AurA inhibition restricts chromatin accessibility of genes associated with inflammatory pathways such as JAK-STAT, TNF, and NF-κB pathways.
View Article and Find Full Text PDFmSphere
September 2025
Department of Biology, Johns Hopkins University, Baltimore, Maryland, USA.
Oxidative stress induces a wide range of cellular damage, often causing disease and cell death. While many organisms are susceptible to the effects of oxidative stress, haloarchaea have adapted to be highly resistant. Several aspects of the haloarchaeal oxidative stress response have been characterized; however, little is known about the impacts of oxidative stress at the translation level.
View Article and Find Full Text PDFJ Integr Neurosci
August 2025
Department of Neurobiology, Hebei Medical University, 050017 Shijiazhuang, Hebei, China.
Background: Sodium homeostasis is crucial for physiological balance, yet the neurobiological mechanisms underlying sodium appetite remain incompletely understood. The nucleus tractus solitarii (NTS) integrates visceral signals to regulate feeding behaviors, including sodium intake. This study investigated the role of 11β-hydroxysteroid dehydrogenase type 2 (HSD2)-expressing neurons in the NTS in mediating sodium appetite under low-sodium diet (LSD) conditions and elucidated the molecular pathways involved, particularly the cyclic adenosine monophosphate (cAMP)/mitogen-activated protein kinase (MAPK) signaling cascade.
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