Background: The aleurone layer is a part of many plant seeds, and during seed germination, aleurone cells undergo PCD, which is promoted by GA from the embryo. However, the numerous components of the GA signaling pathway that mediate PCD of the aleurone layers remain to be identified. Few genes and transcriptomes have been studied thus far in aleurone layers to improve our understanding of how PCD occurs and how the regulatory mechanism functions during PCD. Our previous studies have shown that histone deacetylases (HDACs) are required in GA-induced PCD of aleurone layer. To further explore the molecular mechanisms by which epigenetic modifications regulate aleurone PCD, we performed a global comparative transcriptome analysis of embryoless aleurones treated with GA or histone acetylase (HAT) inhibitors.
Results: In this study, a total of 7,919 differentially expressed genes (DEGs) were analyzed, 2,554 DEGs of which were found to be common under two treatments. These identified DEGs were involved in various biological processes, including DNA methylation, lipid metabolism and ROS signaling. Further investigations revealed that inhibition of DNA methyltransferases prevented aleurone PCD, suggesting that active DNA methylation plays a role in regulating aleurone PCD. GA or HAT inhibitor induced lipoxygenase gene expression, leading to lipid degradation, but this process was not affected by DNA methylation. However, DNA methylation inhibitor could regulate ROS-related gene expression and inhibit GA-induced production of hydrogen peroxide (HO).
Conclusion: Overall, linking of lipoxygenase, DNA methylation, and HO may indicate that GA-induced higher HDAC activity in aleurones causes breakdown of lipids via regulating lipoxygenase gene expression, and increased DNA methylation positively mediates HO production; thus, DNA methylation and lipid metabolism pathways may represent an important and complex signaling network in maize aleurone PCD.
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http://dx.doi.org/10.1186/s12870-023-04565-5 | DOI Listing |
Front Oncol
January 2025
Department of Oncology, Georgetown University Medical Center, Washington, DC, United States.
Cancer's epigenetic landscape, a labyrinthine tapestry of molecular modifications, has long captivated researchers with its profound influence on gene expression and cellular fate. This review discusses the intricate mechanisms underlying cancer epigenetics, unraveling the complex interplay between DNA methylation, histone modifications, chromatin remodeling, and non-coding RNAs. We navigate through the tumultuous seas of epigenetic dysregulation, exploring how these processes conspire to silence tumor suppressors and unleash oncogenic potential.
View Article and Find Full Text PDFJ Endocr Soc
January 2025
Cellular and Molecular Endocrinology Laboratory LIM/25, Division of Endocrinology and Metabolism, Clinicas Hospital, School of Medicine, University of Sao Paulo, 01246-903 Sao Paulo, Brazil.
Human puberty is a dynamic biological process determined by the increase in the pulsatile secretion of GnRH triggered by distinct factors not fully understood. Current knowledge reveals fine tuning between an increase in stimulatory factors and a decrease in inhibitory factors, where genetic and epigenetic factors have been indicated as key players in the regulation of puberty onset by distinct lines of evidence. Central precocious puberty (CPP) results from the premature reactivation of pulsatile secretion of GnRH.
View Article and Find Full Text PDFCureus
January 2025
Neurosurgery, Son Espases University Hospital, Palma, ESP.
Introduction: 5-aminolevulinic acid (5-ALA) fluorescence used in glioma surgery has different intensities within tumors and among different patients, some molecular and external factors have been implicated, but there is no clear evidence analyzing the difference of fluorescence according to glioma molecular characteristics. This study aimed to compare molecular factors of glioma samples with fluorescence intensity to identify potential cofounders and associations with clinically relevant tumor features.
Methods: Tumor samples of high-grade glioma patients operated using 5-ALA for guided resection were included for comparative analysis of fluorescence intensity and molecular features.
Front Microbiol
January 2025
Departments of Otorhinolaryngology-Head and Neck Surgery and Microbiology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, United States.
Oncogenic gamma herpesviruses, including Epstein-Barr Virus (EBV) and Kaposi's Sarcoma-associated Herpesvirus (KSHV), are opportunistic cancer-causing viruses and induces oncogenesis through complex mechanisms, which involves manipulation of cellular physiology as well as epigenetic and epitranscriptomic reprogramming. In this review, we describe the intricate processes by which these viruses interact with the epigenetic machinery, leading to alterations in DNA methylation, histone modifications, and the involvement of non-coding RNAs. The key viral proteins such as EBNA1 and LMP1 encoded by EBV; LANA and vGPCR encoded by KSHV; play pivotal roles in these modifications by interacting with host factors, and dysregulating signaling pathways.
View Article and Find Full Text PDFBMC Med
January 2025
Department of Cardiothoracic Surgery, The Fourth Affiliated Hospital of Soochow University, Suzhou, 215000, China.
Background: Current research underscores the need to better understand the pathogenic mechanisms and treatment strategies for idiopathic pulmonary fibrosis (IPF). This study aimed to identify key targets involved in the progression of IPF.
Methods: We employed Mendelian randomization (MR) with three genome-wide association studies and four quantitative trait loci datasets to identify key driver genes for IPF.
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