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Marine isoprene plays a crucial role in the formation of secondary organic aerosol within the remote marine boundary layer. Due to scarce field measurements of oceanic isoprene and limited laboratory‐based studies of isoprene production, assessing the importance of marine isoprene on atmospheric chemistry and climate is challenging. Calculating in‐field isoprene production rates is a crucial step to predict marine isoprene concentrations and the subsequent emissions to the atmosphere. The distribution, sources, and dominant environmental factors of isoprene were determined in the Northwest Pacific Ocean in 2019. The nutrient enrichment in the Kuroshio Oyashio Extension (KOE) surface seawater, driven by the upwelling and atmospheric deposition, promoted the growth of phytoplankton and elevated the isoprene concentration. This was confirmed by observed responses of isoprene to nutrients and aerosol dust additions in a ship‐based incubation experiment, where the isoprene concentrations increased by 70% (t = 4.417, p < 0.001) and 35% (t = 2.387, p < 0.05), respectively. Biogenic isoprene production rates in the deck incubation experiments were positively related to chlorophyll a, temperature, and solar radiation, with an average production of 7.33 ± 4.27 pmol L−1 day−1. Photochemical degradation of dissolved organic matter was likely an abiotic source of isoprene, contributing to approximately 14% of the total production. Driven by high isoprene production and extreme physical disturbance, the KOE showed very high emissions of isoprene of 46.0 ± 13.0 nmol m−2 day−1, which led to a significant influence on the oxidative capacity of the local atmosphere. Key Points: Nutrient enrichment in the surface seawater driven by upwelling and atmospheric deposition promoted the biological production of isoprenePhotochemical production was confirmed as an abiotic source of marine isopreneApproximately 10%∼63% of net isoprene produced in the mixed layer was transferred to the atmosphere [ABSTRACT FROM AUTHOR]

Tamoxifen is commonly used for the treatment of patients with estrogen receptor‐positive (ER+) breast cancer, but the acquired resistance to tamoxifen presents a critical challenge of breast cancer therapeutics. Recently, long noncoding RNA MIR497HG and its embedded miR‐497 and miR‐195 are proved to play significant roles in many types of human cancers, but their roles in tamoxifen‐resistant breast cancer remain unknown. The results indicate that MIR497HG deficiency induces breast cancer progression and tamoxifen resistance by inducing downregulation of miR‐497/195. miR‐497/195 coordinately represses five positive PI3K‐AKT regulators (MAP2K1, AKT3, BCL2, RAF1, and CCND1), resulting in inhibition of PI3K‐AKT signaling, and PI3K‐AKT inhibition in tamoxifen‐resistant cells restored tamoxifen responsiveness. Furthermore, ER α binds the MIR497HG promoter to activate its transcription in an estrogen‐dependent manner. ZEB1 interacts with HDAC1/2 and DNMT3B at the MIR497HG promoter, resulting in promoter hypermethylation and histone deacetylation. The findings reveal that ZEB1‐induced MIR497HG depletion contributes to breast cancer progression and tamoxifen resistance through PI3K‐AKT signaling. MIR497HG can be used as a biomarker for predicting tamoxifen sensitivity in patients with ER+ breast cancer. [ABSTRACT FROM AUTHOR]

Macrobenthic invertebrates are ubiquitously distributed in the epipelagic zone of the open ocean. Yet, our understanding of their genetic structure patterns remains poorly understood. Investigating the genetic differentiation patterns of pelagic Lepas anatifera and clarifying the potential roles of temperature maintaining this pattern are crucial for our understanding of the distribution and biodiversity of pelagic macrobenthos. In the present study, mitochondrial cytochrome oxidase subunit I (mtDNA COI) from three South China Sea (SCS) populations and six Kuroshio Extension (KE) region populations of L. anatifera sampled from fixed buoys and genome‐wide SNPs from a subset of populations (two SCS populations and four KE region populations) were sequenced and analyzed for investigating the genetic pattern of the pelagic barnacle. Water temperature was different among sampling sites; in other words, the water temperature decreased with latitude increases, and the water temperature on the surface was higher than in the subsurface. Our result showed that three lineages with clear genetic differentiation were found in different geographical locations and depths based on mtDNA COI, all SNPs, neutral SNPs, and outlier SNPs. Lineage 1 and lineage 2 were dominant in the subsurface populations and surface populations from the KE region, respectively. Lineage 3 was dominant in the SCS populations. Historical events during the Pliocene epoch shaped the differentiation of the three lineages, while, nowadays, temperature heterogeneity maintains the current genetic pattern of L. anatifera in the northwest Pacific. The subsurface populations were genetically isolated from the surface populations in the Kuroshio Extension (KE) region, implying small‐scale vertical thermal heterogeneity was also an important factor maintaining the genetic differentiation pattern of the pelagic species. [ABSTRACT FROM AUTHOR]

Background: Breast cancer remains the most common malignancy in females around the world. Recently, a growing number of studies have focused on gene dysregulation. In our previous study, Krüppel‐like factors (KLFs) were found to play essential roles in breast cancer development, among which KLF2 could function as a tumor suppressor. Nevertheless, the underlying molecular mechanism remains unclear. Methods: miR‐92a‐3p was identified as the upstream regulator of KLF2 by starBase v.3.0. The regulation of KLF2 by miR‐92a‐3p was verified by a series of in vitro and in vivo assays. Further exploration revealed that Baculoviral IAP Repeat Containing 5 (BIRC5) was the target of KLF2. ChIP assay, dual‐luciferase reporter analysis, quantitative real‐time PCR, and western blot were performed for verification. Results: miR‐92a‐3p functioned as a tumor promoter by inhibiting KLF2 by binding to its 3'‐untranslated region (3'‐UTR). In addition, KLF2 could transcriptionally suppress the expression of BIRC5. Conclusion: Collectively, our results uncovered the miR‐92a‐3p/KLF2/BIRC5 axis in breast cancer and provided a potential mechanism for breast cancer development, which may serve as promising strategies for breast cancer therapy. [ABSTRACT FROM AUTHOR]

Arylalkylamine N‐acetyltransferase (aaNAT) catalyzes the acetylation of dopamine, 5‐hydroxy‐tryptamine, tryptamine, octopamine, norepinephrine and other arylalkylamines to form respective N‐acetyl‐arylalkylamines. Depending on the products formed, aaNATs are involved in a variety of physiological functions. In the yellow fever mosquito, Aedes aegypti, a number of aaNATs and aaNAT‐like proteins have been reported. However, the primary function of each individual aaNAT is yet to be identified. In this study we investigated the function of Ae. aegypti aaNAT1 (Ae‐aaNAT1) in cuticle pigmentation and development of morphology. Ae‐aaNAT1 transcripts were detected at all stages of development with highest expressions after pupation and right before adult eclosion. Ae‐aaNAT1 mutant mosquitoes generated using clustered regularly interspaced palindromic repeats (CRISPR) – CRISPR‐associated protein 9 had no obvious effect on larval and pupal development. However, the mutant mosquitoes exhibited a roughened exoskeletal surface, darker cuticles, and color pattern changes suggesting that Ae‐aaNAT1 plays a role in development of the morphology and pigmentation of Ae. aegypti adult cuticles. The mutant also showed less blood feeding efficiency and lower fecundity when compared with the wild‐type. The mutation of Ae‐aaNAT1 influenced expression of genes involved in cuticle formation. In summary, Ae‐aaNAT1 mainly functions on cuticular pigmentation and also affects blood feeding efficiency and fecundity. [ABSTRACT FROM AUTHOR]

Cordycepin, an adenosine analog, has been reported to improve cognitive function, but which seems to be inconsistent with the reports showing that cordycepin inhibited long‐term potentiation (LTP). Behavioral‐LTP is usually used to study long‐term synaptic plasticity induced by learning tasks in freely moving animals. In order to investigate simultaneously the effects of cordycepin on LTP and behavior in rats, we applied the model of behavioral‐LTP induced by Y‐maze learning task through recording population spikes in hippocampal CA1 region. Golgi staining and Sholl analysis were employed to assess the morphological structure of dendrites in pyramidal cells of hippocampal CA1 area, and western blotting was used to examine the level of adenosine A1 receptors and A2A receptors (A2AR). We found that cordycepin significantly improved behavioral‐LTP magnitude, accompanied by increases in the total length of dendrites, the number of intersections and spine density but did not affect Y‐maze learning task. Furthermore, cordycepin obviously reduced A2AR level without altering adenosine A1 receptors level; and the agonist of A2AR (CGS 21680) rather than antagonist (SCH 58261) could reverse the potentiation of behavioral‐LTP induced by cordycepin. These results suggested that cordycepin improved behavioral‐LTP and morphological structure of dendrite in hippocampal CA1 but did not contribute to the improvement of learning and memory. And cordycepin improved behavioral‐LTP may be through reducing the level of A2AR in hippocampus. Collectively, the effects of cordycepin on cognitive function and LTP were complex and involved multiple mechanisms. [ABSTRACT FROM AUTHOR]