Search

Shoot stem cells act as the source of the aboveground parts of flowering plants. A precise regulatory basis is required to ensure that plant stem cells show the right status during the stages of proliferation, senescence and cell death. Over the past few decades, the genetic circuits controlling stem cell fate, including the regulatory pathways of establishment, maintenance and differentiation, have been largely revealed. However, the morphological changes and molecular mechanisms of the final stages of stem cells, which are represented by senescence and cell death, have been less studied. The senescence and death of shoot stem cells are under the control of a complex series of pathways that integrate multiple internal and external signals. Given the crucial roles of shoot stem cells in influencing plant longevity and crop yields, researchers have attempted to uncover details of stem cell senescence and death. Recent studies indicate that stem cell activity arrest is controlled by the FRUITFULL–APETALA2 pathway and the plant hormones auxin and cytokinin, while the features of senescent and dead shoot apical stem cells have also been described, with dynamic changes in reactive oxygen species implicated in stem cell death. In this review, we highlight the recent breakthroughs that have enriched our understanding of senescence and cell death processes in plant stem cells. [ABSTRACT FROM AUTHOR]

Thermosensitive genic male sterile (TGMS) wheat lines are the core of two-line hybrid systems. Understanding the mechanism that regulates male sterility in TGMS wheat lines is helpful for promoting wheat breeding. Several studies have obtained information regarding the mechanisms associated with male sterility at the transcriptional level, but it is not clear how the post-transcriptional process of alternative splicing might contribute to controlling male sterility. In this study, we performed genome-wide analyses of alternative splicing during the meiosis stage in TGMS line BS366 using PacBio and RNA-Seq hybrid sequencing. Cytological observations indicated that cytoskeleton assembly in pollen cells, calcium deposition in pollen and tapetal cells, and vesicle transport in tapetal cells were deficient in BS366. According to our cytological findings, 49 differentially spliced genes were isolated. Moreover, 25 long non-coding RNA targets and three bHLH transcription factors were identified. Weighted gene co-expression network analysis detected four candidate differentially spliced genes that had strong co-relation with the seed setting percentage, which is the direct representation of male sterility in BS366. In this study, we obtained comprehensive data regarding the alternative splicing-mediated regulation of male sterility in TGMS wheat. The candidates identified may provide the molecular basis for an improved understanding of male sterility. [ABSTRACT FROM AUTHOR]

Nonribosomal peptide synthetases (NRPSs) are multi-modular enzymes involved in the biosynthesis of natural products. Bacillamide C was synthesized by Bacillus atrophaeus C89. A nonribosomal peptide synthetase (NRPS) cluster found in the genome of B. atrophaeus C89 was hypothesized to be responsible for the biosynthesis of bacillamide C using alanine and cysteine as substrates. Here, the structure analysis of adenylation domains based on homologous proteins with known crystal structures indicated locations of the substrate-binding pockets. Molecular docking suggested alanine and cysteine as the potential substrates for the two adenylation domains in the NRPS cluster. Furthermore, biochemical characterization of the purified recombinant adenylation domains proved that alanine and cysteine were the optimum substrates for the two adenylation domains. The results provided the in vitro evidence for the hypothesis that the two adenylation domains in the NRPS of B. atrophaeus C89 preferentially select alanine and cysteine, respectively, as a substrate to synthesize bacillamide C. Furthermore, this study on substrates selectivity of adenylation domains provided basis for rational design of bacillamide analogs. [ABSTRACT FROM AUTHOR]

Metabolism refers to a series of orderly chemical reactions used to maintain life activities in organisms. In healthy individuals, metabolism remains within a normal range. However, specific diseases can lead to abnormalities in the levels of certain metabolites, causing them to either increase or decrease. Detecting these deviations in metabolite levels can aid in diagnosing a disease. Traditional biological experiments often rely on a lot of manpower to do repeated experiments, which is time consuming and labor intensive. To address this issue, we develop a deep learning model based on the auto-encoder and non-negative matrix factorization named as MDA-AENMF to predict the potential associations between metabolites and diseases. We integrate a variety of similarity networks and then acquire the characteristics of both metabolites and diseases through three specific modules. First, we get the disease characteristics from the five-layer auto-encoder module. Later, in the non-negative matrix factorization module, we extract both the metabolite and disease characteristics. Furthermore, the graph attention auto-encoder module helps us obtain metabolite characteristics. After obtaining the features from three modules, these characteristics are merged into a single, comprehensive feature vector for each metabolite–disease pair. Finally, we send the corresponding feature vector and label to the multi-layer perceptron for training. The experiment demonstrates our area under the receiver operating characteristic curve of 0.975 and area under the precision–recall curve of 0.973 in 5-fold cross-validation, which are superior to those of existing state-of-the-art predictive methods. Through case studies, most of the new associations obtained by MDA-AENMF have been verified, further highlighting the reliability of MDA-AENMF in predicting the potential relationships between metabolites and diseases. [ABSTRACT FROM AUTHOR]

The chloroplast is a semi-autonomous organelle with a double membrane structure, and its structural stability is a prerequisite for its correct function. Chloroplast development is regulated by known nuclear-encoded chloroplast proteins or proteins encoded within the chloroplast itself. However, the mechanism of chloroplast development regulated by other organelles remains largely unknown. Here, we report that the nuclear-localized DEAD-box RNA helicase 13 (RH13) is essential for chloroplast development in Arabidopsis thaliana. RH13 is widely expressed in tissues and localized to the nucleolus. A homozygous rh13 mutant shows abnormal chloroplast structure and leaf morphogenesis. Proteomic analysis showed that the expression levels of photosynthesis-related proteins in chloroplasts were reduced due to loss of RH13. Furthermore, RNA-sequencing and proteomics data revealed decreases in the expression levels of these chloroplast-related genes, which undergo alternative splicing events in the rh13 mutant. Taken together, we propose that nucleolus-localized RH13 is critical for chloroplast development in Arabidopsis. [ABSTRACT FROM AUTHOR]

The transcription factor signal transducer and activator of transcription 3 (STAT3) contributes to cell proliferation, apoptosis and motility in human cancer cells. We aim to elucidate the function of STAT3 in esophageal carcinogenesis process and molecular mechanisms. We showed that hyperactivated STAT3 in esophageal carcinogenesis tissues correlated with the overexpression of octamer transcription factor-1 (Oct-1). High STAT3 phosphorylation correlated with shorter survival compared with low STAT3 phosphorylation. STAT3 and Oct-1 expression levels affected the proliferation and colony formation of Eca-109 esophageal squamous cell carcinoma cells by altering Erk and Akt activation. Nevertheless, STAT3 regulated the migration and invasion of esophageal squamous cell carcinoma cells independent of Oct-1. In conjunction with Oct-1, STAT3 inhibited apoptosis in esophageal squamous cell carcinoma cells. Constitutively activated STAT3 in normal human esophageal epithelium cells (HET-1A) elevated Oct-1 expression,and promoted proliferation and decreased apoptosis. STAT3 activated HET-1A cells to form tumors in vivo, suggesting that overactivated STAT3 is sufficient for carcinogenesis. We further confirmed the colocalization of STAT3 and Oct-1 in the nucleus and found that STAT3 regulates the transcription and expression of Oct-1 by directly targeting its promoter. Activated STAT3 also upregulated many genes associated with Oct-1. Together, our results indicate that STAT3 plays a crucial role in esophageal carcinogenesis by regulating the cell proliferation and apoptosis in conjunction with Oct-1. [ABSTRACT FROM AUTHOR]