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Abstract Interspecific genomic introgression is an important evolutionary process with respect to the generation of novel phenotypic diversity and adaptation. A key question is how gene flow perturbs gene expression networks and regulatory interactions. Here, an introgression population of two species of allopolyploid cotton (Gossypium) to delineate the regulatory perturbations of gene expression regarding fiber development accompanying fiber quality change is utilized. De novo assembly of the recipient parent (G. hirsutum Emian22) genome allowed the identification of genomic variation and introgression segments (ISs) in 323 introgression lines (ILs) from the donor parent (G. barbadense 3–79). It documented gene expression dynamics by sequencing 1,284 transcriptomes of developing fibers and characterized genetic regulatory perturbations mediated by genomic introgression using a multi‐locus model. Introgression of individual homoeologous genes exhibiting extreme low or high expression bias can lead to a parallel expression bias in their non‐introgressed duplicates, implying a shared yet divergent regulatory fate of duplicated genes following allopolyploidy. Additionally, the IL N182 with improved fiber quality is characterized, and the candidate gene GhFLAP1 related to fiber length is validated. This study outlines a framework for understanding introgression‐mediated regulatory perturbations in polyploids, and provides insights for targeted breeding of superior upland cotton fiber.

Cracks, common indicators of deterioration in bridge frameworks, frequently stem from wear and rust, leading to increased local flexibility and changes in the structure’s dynamic behavior. This study examines how these cracks affect the dynamics of footbridges when subjected to loads generated by walking individuals. The pedestrian is modeled as a linear oscillator, while the cracked bridge is represented by a simply supported beam following Euler–Bernoulli’s theory. The use of the Dirac delta function allows for the precise representation of the localized stiffness reduction at the crack location, facilitating the calculation of analytical expressions for the beam’s vibration modes. The research suggests that the presence of cracks minimally affects the bridge’s mid-span displacement. However, with a limited depth of cracks, the appearance of cracks notably amplifies the mid-span acceleration amplitude of the bridge, leading to a pronounced concentration of energy at the third natural frequency of the bridge in the acceleration spectrum. As the depth and number of cracks increase, the acceleration amplitude continues to decrease, but the corresponding spectrum remains almost unchanged. The study’s outcomes enhance the comprehension of how cracks affect the performance of bridge structures when subjected to loads from pedestrians, offering insights for the monitoring and evaluation of the condition of cracked footbridges.

Abstract An understanding of the mechanisms regulating embryonic hematopoietic stem cell (HSC) development would facilitate their regeneration. The aorta-gonad-mesonephros region is the site for HSC production from hemogenic endothelial cells (HEC). While several distinct regulators are involved in this process, it is not yet known whether macroautophagy (autophagy) plays a role in hematopoiesis in the pre-liver stage. Here, we show that different states of autophagy exist in hematopoietic precursors and correlate with hematopoietic potential based on the LC3-RFP-EGFP mouse model. Deficiency of autophagy-related gene 5 (Atg5) specifically in endothelial cells disrupts endothelial to hematopoietic transition (EHT), by blocking the autophagic process. Using combined approaches, including single-cell RNA-sequencing (scRNA-seq), we have confirmed that Atg5 deletion interrupts developmental temporal order of EHT to further affect the pre-HSC I maturation, and that autophagy influences hemogenic potential of HEC and the formation of pre-HSC I likely via the nucleolin pathway. These findings demonstrate a role for autophagy in the formation/maturation of hematopoietic precursors.

Neuraminidase inhibitors (NAIs) are the mainstay antiviral drugs against influenza infection. In this study, a ligand fishing protocol was developed to screen NAIs using neuraminidase immobilized magnetic beads (NA-MB). After verifying the feasibility of NA-MB with an artificial mixture including NA inhibitors and non-inhibitors, the developed ligand fishing protocol was applied to screen NAIs from the crude extracts of Duchesnea indica Andr. Twenty-four NA binding compounds were identified from the normal butanol (n-BuOH) extract of D. indica as potential NAIs by high-performance liquid chromatography coupled with quadrupole time-of-flight mass spectrometry (HPLC–Q-TOF-MS) assisted with Compound Structure Identification (CSI):FingerID, including 12 ellagitannins, 4 brevifolin derivatives, 3 ellagic acid derivatives, and 4 flavonoids. Among them, 9 compounds were isolated and tested for in vitro NA inhibitory activities against NA from Clostridium perfringens, and from oseltamivir sensitive and resistant influenza A virus strains. The results indicate that compound B23 has the NA inhibitory activities in both the oseltamivir sensitive and resistant viral NA, with half maximal inhibitory concentration (IC50) values of 197.9 and 125.4 μmol/L, respectively. Moreover, B23 can obviously reduce the replication of oseltamivir sensitive and resistant viruses in Madin–Darby canine kidney (MDCK) cells at the concentrations of 40 and 200 μmol/L.