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Arbuscular mycorrhiza (AM) is a widespread symbiosis between plant roots and fungi of the Glomeromycotina, which improves nutrient uptake by plants. The molecular mechanisms underlying development and function of the symbiosis are subject to increasing research activity. Since AM occurs in the soil, most studies targeting a molecular understanding of AM development and function, use solid substrates for co-cultivating plants and AM fungi. However, for some experiments very clean roots, highly controlled nutrient conditions or applications of defined concentrations of signaling molecules (such as hormones) or other small chemicals (such as synthetic inhibitors or signaling agonists) are needed. Etoposide To this end, hydroponics has been widely used in research on mechanisms of plant nutrition and some hydroponic systems were developed for AM fungal spore amplification. Here, we present a hydroponics set-up, which can be successfully utilized for experimental root colonization assays. We established a "tip-wick" system based on pipette tips and rock wool wicks for co-cultivation of AM fungi with small model plants such as Lotus japonicus. A larger "Falcon-wick" system using Falcon tubes and rockwool wicks was developed for larger model plants such as rice. The hydroponic system can also be employed for growing L. japonicus hairy roots after transformation by Agrobacterium rhizogenes, thus circumventing the laborious cultivation on agar medium-containing Petri dishes during hairy root development. The tip-wick and Falcon-wick systems are easy to use and can be built with low cost, conventional and reusable lab plastic ware and a simple aquarium pump. Copyright © 2020 Das, Torabi, Chapman and Gutjahr.Secondary metabolites of the flavonoid pathway participate in plant defense, and bHLH and MYB transcription factors regulate the synthesis of these metabolites. Here, we define the regulatory mechanisms in response to pathogens. Two transcription factors from Populus alba var. pyramidalis, PalbHLH1 and PalMYB90, were overexpressed together in poplar, and transcriptome analysis revealed differences in response to pathogen infection. The transgenic plants showed elevated levels of several key flavonoid pathway components total phenols, proanthocyanidins (PAs), and anthocyanins and intermediates quercetin and kaempferol. Furthermore, PalbHLH1 and PalMYB90 overexpression in poplar enhanced antioxidase activities and H2O2 release and also increased resistance to Botrytis cinerea and Dothiorella gregaria infection. Gene expression profile analysis showed most genes involved in the flavonoid biosynthesis pathway or antioxidant response to be upregulated in MYB90/bHLH1-OE poplar, but significant differential expression occurred in response to pathogen infection. Specifically, expression of PalF3H (flavanone 3-hydroxylase), PalDFR (dihydroflavonol 4-seductase), PalANS (anthocyanin synthase), and PalANR (anthocyanin reductase), which function in initial, middle, and final steps of anthocyanin and PA biosynthesis, respectively, was significantly upregulated in D. gregaria-infected MYB90/bHLH1-OE poplar. Our results highlight that PalbHLH1 and PalMYB90 function as transcriptional activators of flavonoid pathway secondary-metabolite synthesis genes, with differential mechanisms in response to bacterial or fungal infection. Copyright © 2020 Bai, Duan, Ma, Fen, Sun, Long, Lv and Wan.Therapeutic targeting of IL-17A and its receptor IL-17RA with antibodies has turned out to be a tremendous success in the treatment of several autoimmune conditions. As the IL-17 cytokine family consists of six members (IL-17A to F), it is intriguing to elucidate the biological function of these five other molecules to identify more potential targets. In the past decade, IL-17C has emerged as quite a unique member of this pro-inflammatory cytokine group. In contrast to the well-described IL-17A and IL-17F, IL-17C is upregulated at very early timepoints of several disease settings. Also, the cellular source of the homodimeric cytokine differs from the other members of the family Epithelial rather than hematopoietic cells were identified as the producers of IL-17C, while its receptor IL-17RE is expressed on TH17 cells as well as the epithelial cells themselves. Numerous investigations led to the current understanding that IL-17C (a) maintains an autocrine loop in the epithelium reinforcing innate immune barriers and (b) stimulates highly inflammatory TH17 cells. Functionally, the IL-17C/RE axis has been described to be involved in the pathogenesis of several diseases ranging from infectious and autoimmune conditions to cancer development and progression. This body of evidence has paved the way for the first clinical trials attempting to neutralize IL-17C in patients. Here, we review the latest knowledge about identification, regulation, and function of the IL-17C/IL-17receptor E pathway in inflammation and immunity, with a focus on the mechanisms underlying tissue injury. We also discuss the rationale for the translation of these findings into new therapeutic approaches in patients with immune-mediated disease. Copyright © 2020 Nies and Panzer.In the context of adoptive T cell transfer (ACT) for cancer treatment, it is crucial to generate in vitro large amounts of tumor-specific CD8 T cells with high potential to persist in vivo. PD-1, Tim3, and CD39 have been proposed as markers of tumor-specific tumor-infiltrating CD8 T lymphocytes (CD8 TILs). However, these molecules are highly expressed by terminally differentiated exhausted CD8 T cells (Tex) that lack proliferation potential. Therefore, optimized strategies to isolate tumor-specific TILs with high proliferative potential, such as Tcf1+ precursor exhausted T cells (Tpe) are needed to improve in vivo persistence of ACT. Here we aimed at defining cell surface markers that would unequivocally identify Types for precision cell sorting increasing the purity of tumor-specific PD-1+ Tcf1+ Tpe from total TILs. Transcriptomic analysis of Tpe vs. Tex CD8 TIL subsets from B16 tumors and primary human melanoma tumors revealed that Tpes are enriched in Slamf6 and lack Entpd1 and Havcr2 expression, which encode Slamf6, CD39, and Tim3 cell surface proteins, respectively.

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