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In the natural ecosystem, plants usually grow at high vegetation density for yield maximization. The high‐density planting triggers a variety of strategies to avoid canopy shade and competes with their neighbors for light and nutrition, which are collected termed shade avoidance responses. The molecular mechanism underlying shade avoidance and nutrition has expanded largely in the past decade; however, how these two responses intersect remains poorly understood. Here, we show that simulated shade undermined Pi starvation response and the phytohormone JA is involved in this process. We found that the JA signaling repressor JAZ proteins directly interact with PHR1 to repress its transcriptional activity on downstream targets, including phosphate starvation induced genes. Furthermore, FHY3 and FAR1, the negative regulators of shade avoidance, directly bind to promoters of NIGT1.1 and NIGT1.2 to activate their expression, and this process is also antagonized by JAZ proteins. All these results finally result in attenuation of Pi starvation response under shade and Pi‐depleted conditions. Our findings unveil a previously unrecognized molecular framework whereby plants integrate light and hormone signaling to modulate phosphate responses under plant competition. [ABSTRACT FROM AUTHOR]

Background and Aim: Although endoscopic ultrasound‐guided fine‐needle biopsy is widely applied, there is no clear consensus on the optimal biopsy technique. We described a modified wet suction technique (MWEST) with the aim to compare the efficacy and safety between MWEST and the dry suction technique (DST). Methods: In this prospective, randomized, crossover, single‐blinded study, patients with suspected pancreatic malignancy were randomized to the DST (group A) or MWEST (group B) for the first pass, and the two techniques were performed alternately. The primary outcome was the comparison of specimen adequacy and diagnostic yield between the techniques. Secondary outcomes included the macroscopic visible core length, blood contamination of specimens, and adverse events of both techniques. Results: From January 2019 to September 2019, 216 passes were performed in 50 patients. The specimen adequacy was significantly higher in "per‐lesion" (P = 0.026), "per‐pass" (cytology: P = 0.034; histology: P = 0.042), and first‐pass analysis (P = 0.034) for MWEST than for DST. In diagnostic yield, MWEST showed significantly superior histological yield (P = 0.014) and first‐pass analysis (κ: MWEST: 0.743 and DST: 0.519) compared with DST. The median macroscopic visible core lengths were 8 mm (interquartile range: 3.25–15 mm) and 10 mm (interquartile range: 5.25–15 mm) for DST and MWEST, respectively (P = 0.036). Blood contamination was significantly more serious in DST than in MWEST (cytology: P = 0.021; histology: P = 0.042). Conclusions: Endoscopic ultrasound‐guided fine‐needle biopsy with MWEST resulted in significantly better quality of specimen, histological, and first‐pass diagnostic yields and comparable safety compared with the DST. MWEST is preferred for endoscopic ultrasound‐guided fine‐needle biopsy in pancreatic solid lesions. [ABSTRACT FROM AUTHOR]

Inflammatory bowel disease (IBD), which includes ulcerative colitis (UC) and Crohn's disease (CD), has a complex etiology that may be associated with dysbiosis of the microbiota. Previously, our study revealed significant loss of Roseburia intestinalis from the gut of untreated patients with CD, and that R. intestinalis exerted anti-inflammatory functions in TNBS-induced colitis; however, the function of R. intestinalis supernatant is unknown. Therefore, LPS-induced macrophages, including RAW264.7 macrophages and bone marrow-derived macrophages were treated with R. intestinalis supernatant. The results indicated that R. intestinalis supernatant suppressed expression of interleukin (IL)-6 and signal transducer and activator of transcription 3 (STAT3) by macrophages. Additionally, these findings were further verified in vivo in DSS- and TNBS-induced mouse models of colitis. It was observed that R. intestinalis supernatant ameliorated IBD colitis by reducing the number of inflammatory macrophages and Th17 cells in the colon, and by downregulating the expression of IL-6 and STAT3. Finally, the non-protein components of R. intestinalis supernatant were examined using gas chromatography-mass spectrometry analysis and identified the presence of short-chain fatty acids. In conclusion, the results of the present study indicated that R. intestinalis supernatant may regulate immune responses and ameliorate colitis. [ABSTRACT FROM AUTHOR]

Anthocyanins affect quality in fruits such as grape (Vitis vinifera). High temperatures reduce anthocyanin levels by suppressing the expression of anthocyanin biosynthesis genes and decreasing the biosynthetic rate. However, the regulatory mechanisms that coordinate these two processes remain largely unknown. In this study, we demonstrate that high-temperature-mediated inhibition of anthocyanin biosynthesis in grape berries depends on the auxin and endoplasmic reticulum (ER) stress pathways. Inactivation of these pathways restores anthocyanin accumulation under high temperatures. We identified and characterized FAR-RED ELONGATED HYPOCOTYL3 (FHY3), a high-temperature-modulated transcription factor that activates multiple anthocyanin biosynthesis genes by binding to their promoters. The auxin response factor VvARF3 interacts with VvFHY3 and represses its transactivation activity, antagonizing VvFHY3-induced anthocyanin biosynthesis. Additionally, we found that the ER stress sensor VvbZIP17 represses anthocyanin biosynthesis. VvFHY3 suppresses VvbZIP17 activity by directly binding to the VvbZIP17 promoter to repress its transcription and by physically interacting with VvbZIP17 to block its DNA binding ability. Furthermore, AUXIN RESPONSE FACTOR 3 (ARF3) interferes with the VvFHY3-VvbZIP17 interaction, releasing VvbZIP17 to activate the unfolded protein response and further suppress anthocyanin production. Our results unravel the VvARF3-VvFHY3-VvbZIP17 regulatory module, which links the auxin and ER stress pathways to coordinately repress anthocyanin structural gene expression and biosynthesis under high-temperature stress., (© The Author(s) 2024. Published by Oxford University Press on behalf of American Society of Plant Biologists. All rights reserved. For commercial re-use, please contact reprints@oup.com for reprints and translation rights for reprints. All other permissions can be obtained through our RightsLink service via the Permissions link on the article page on our site—for further information please contact journals.permissions@oup.com.)

Ulcerative colitis (UC) is a type of inflammatory bowel disease (IBD), which is a chronic, relapsing condition associated with the disorder of gut microbial communities. A previous study reported that levels of Roseburia intestinalis (R.I), a butyrate‑producing bacterium, are significantly decreased in patients with IBD and exert an anti‑inflammatory function in dextran sulfate sodium (DSS)‑induced colitis. However, the role of R.I flagellin in UC and its underlying molecular mechanism are not yet fully understood. Therefore, a DSS‑induced colitis model in C57Bl/6 mice and the LPS/ATP‑induced THP‑1 macrophages were treated with R.I flagellin, which were used to investigate the anti‑inflammatory effects of R.I flagellin. The results demonstrated that R.I flagellin decreased colitis‑associated disease activity index, colonic shortening and the pathological damage of the colon tissues in murine colitis models. Furthermore, R.I flagellin decreased the serum levels of proinflammatory cytokines and inhibited activation of the nucleotide‑binding oligomerization segment‑like receptor family 3 (NLRP3) inflammasome in murine colitis. R.I flagellin was also demonstrated to decrease the Gasdermin D to yield the N‑terminal fragment membrane pore and inhibit inflammasome‑triggered pyroptosis. In vitro analysis indicated that microRNA (miR)‑223‑3p was involved in the regulation of R.I flagellin on NLRP3 inflammasome activation. Taken together, the results of the present study demonstrated that R.I flagellin inhibited activation of the NLRP3 inflammasome and pyroptosis via miR‑223‑3p/NLRP3 signaling in macrophages, suggesting that R.I flagellin may be used as a novel probiotic product for the treatment of UC.