Cassava (Manihot esculenta Crantz) is an important crop with a high photosynthetic rate and high yield. It is classified as a C3–C4 plant based on its photosynthetic and structural characteristics. To investigate the structural and photosynthetic characteristics of cassava leaves at the cellular level, we created a single-cell transcriptome atlas of cassava leaves. A total of 11,177 high-quality leaf cells were divided into 15 cell clusters. Based on leaf cell marker genes, we identified 3 major tissues of cassava leaves, which were mesophyll, epidermis, and vascular tissue, and analyzed their distinctive properties and metabolic activity. To supplement the genes for identifying the types of leaf cells, we screened 120 candidate marker genes. We constructed a leaf cell development trajectory map and discovered 6 genes related to cell differentiation fate. The structural and photosynthetic properties of cassava leaves analyzed at the single cellular level provide a theoretical foundation for further enhancing cassava yield and nutrition.

Alzheimer’s disease (AD) is a progressive neurodegenerative disorder associated with synaptic dysfunction, pathological accumulation of β‐amyloid peptide 1‐42 (Aβ _1‐42 ), and neuronal loss. The self‐association of Aβ _1‐42 monomers (Aβ‐M) into soluble oligomers seems to be crucial for the development of neurotoxicity. Previous publications have shown that Aβ oligomers and dimers might play key roles in inducing AD. The role of Aβ‐M was rarely investigated and still unclear in AD. To understand the effects of Aβ‐M on neurons and other cell types in the brain could be the key to understand its function. In our study, we found that Aβ‐M expression slowly induced cell apoptosis within 48 hours after transfection, β2 adrenergic receptor (β2AR) interacted with Aβ‐M in the pull‐down and the yeast two‐hybrid assays, and Aβ‐M played a major role in inducing phosphorylation of Tau at Ser‐214, c‐Jun N‐terminal kinase (JNK) at Thr‐183/Tyr‐185, p70 ribosomal protein S6 kinase (p70S6K) at Thr‐389. We also discovered that β2AR, G protein‐coupled receptor kinase 2 (GRK2), and protein kinase A (PKA) mediated the phosphorylation of Tau and JNK. Aβ‐M induced phosphorylation of Tau at Ser‐214 through both β2AR‐cAMP/PKA‐JNK and β2AR‐GRK signaling pathways. Mitogen‐activated protein kinase kinase (MEK) mediated the phosphorylation of p70S6K induced by Aβ‐M.

Osteoporosis (OP) is a systemic bone disease with loss of bone mass and destruction of the microscopic structure. Many antiosteoporosis drugs have been used for OP therapy, but the therapeutic efficiency remains limited. Therefore, there is an urgent need to develop new drugs for antiosteoporosis treatment. Selenium (Se) is one kind of essential trace element for humans and displays pivotal roles in maintaining bone homeostasis. However, the modulation roles of Se are greatly affected by its chemical forms. Herein, Se containing protein derived from Se-enriched Spirulina platensis (Se-SP) were extracted and used for the treatment of OP in an ovariectomized mice model. The results showed that Se-SP showed enhanced potential in promoting excretion of calcium and alkaline phosphatase (ALP) expression than that of SP in MC3T3-E1 cells. Micro-CT revealed that Se-SP administration in vivo effectively alleviated bone loss as indicated by the upregulated BV, Tb.Th, Bv/TV, Tb.N, and BMD as well as the decreased Tb.Sp. Se-SP in vivo also significantly suppressed inflammatory response through restricting the expression of proinflammatory cytokines expression and upregulating the secretion of anti-inflammatory cytokines. Additionally, Se-SP effectively inhibited ovariectomy-induced osteoblast inactivation and osteoclastogenesis by upregulating BMP2, RUNX2, COL-I, OCN and OPG pression and downregulating RANKL expression. Together, these findings suggested that Se-SP was a new form of Se in therapy of human OP.

Alzheimer’s disease (AD) is an intractable and progressive neurodegenerative disease. Amyloid beta (Aβ) aggregation is the hallmark of AD. Aβ induces neurotoxicity through a variety of mechanisms, including interacting with membrane receptors to alter downstream signaling, damaging cellular or organelle membranes, interfering with protein degradation and synthesis, and inducing an excessive immune-inflammatory response, all of which lead to neuronal death and other pathological changes associated with AD. In this study, we extracted gene expression profiles from the GSE5281 and GSE97760 microarray datasets in the GEO (Gene Expression Omnibus) database, as well as from the Human Gene Database. We identified differentially expressed genes in the brain tissues of AD patients and healthy persons. Through GO, KEGG, and ROC analyses, annexin A2 (AnxA2) was identified as a putative target gene. Notably, accumulating evidence suggests that intracellular AnxA2 is a key regulator in various biological processes, including endocytosis, transmembrane transport, neuroinflammation, and apoptosis. Thus, we conducted a series of cell biology experiments to explore the biological function of AnxA2 in AD. The results indicate that AnxA2 gene knockdown primarily affects oxidative phosphorylation, cell cycle, AD, protein processing in the endoplasmic reticulum, SNARE interactions in vesicular transport, and autophagy. In SH-SY5Y cells secreting Aβ42, AnxA2 gene knockdown exacerbated Aβ42-induced cytotoxicity, including cell death, intracellular ROS levels, and neuronal senescence, altered cell cycle, and reduced ATP levels, suggesting its critical role in mitochondrial function maintenance. AnxA2 gene knockdown also exacerbated the inhibitory effect of Aβ42 on cell migration. AnxA2 overexpression reduced the inflammatory response induced by Aβ42, while its absence increased pro-inflammatory and decreased anti-inflammatory responses. Furthermore, AnxA2 gene knockdown facilitated apoptosis and decreased autophagy. These results indicated potential pathophysiological roles of AnxA2 in AD.

The major pathological feature of Alzheimer’s disease (AD) is the aggregation of amyloid β peptide (Aβ) in the brain. Inhibition of Aβ₄₂ aggregation may prevent the advancement of AD. This study employed molecular dynamics, molecular docking, electron microscopy, circular dichroism, staining of aggregated Aβ with ThT, cell viability, and flow cytometry for the detection of reactive oxygen species (ROS) and apoptosis. Aβ₄₂ polymerizes into fibrils due to hydrophobic interactions to minimize free energy, adopting a β-strand structure and forming three hydrophobic areas. Eight dipeptides were screened by molecular docking from a structural database of 20 L-α-amino acids, and the docking was validated by molecular dynamics (MD) analysis of binding stability and interaction potential energy. Among the dipeptides, arginine dipeptide (RR) inhibited Aβ₄₂ aggregation the most. The ThT assay and EM revealed that RR reduced Aβ₄₂ aggregation, whereas the circular dichroism spectroscopy analysis showed a 62.8% decrease in β-sheet conformation and a 39.3% increase in random coiling of Aβ₄₂ in the presence of RR. RR also significantly reduced the toxicity of Aβ₄₂ secreted by SH-SY5Y cells, including cell death, ROS production, and apoptosis. The formation of three hydrophobic regions and polymerization of Aβ₄₂ reduced the Gibbs free energy, and RR was the most effective dipeptide at interfering with polymerization.

Maximizing cell survival under stress requires rapid and transient adjustments of RNA and protein synthesis. However, capturing these dynamic changes at both single-cell level and across an organism has been challenging. Here, we developed a system named MONITTR (MS2-embedded mCherry-based monitoring of transcription) for real-time simultaneous measurement of nascent transcripts and endogenous protein levels in C. elegans. Utilizing this system, we monitored the transcriptional bursting of fasting-induced genes and found that the epidermis responds to fasting by modulating the proportion of actively transcribing nuclei and transcriptional kinetics of individual alleles. Additionally, our findings revealed the essential roles of the transcription factors NHR-49 and HLH-30 in governing the transcriptional kinetics of fasting-induced genes under fasting. Furthermore, we tracked transcriptional dynamics during heat-shock response and ER unfolded protein response and observed rapid changes in the level of nascent transcripts under stress conditions. Collectively, our study provides a foundation for quantitatively investigating how animals spatiotemporally modulate transcription in various physiological and pathological conditions.