Biomineralization is one of the key processes that is notably affected in marine calcifiers such as oysters under ocean acidification (OA). Understanding molecular changes in the biomineralization process under OA and its heritability, therefore, is key to developing conservation strategies for protecting ecologically and economically important oyster species. To do this, in this study, we have explicitly chosen the tissue involved in biomineralization (mantle) of an estuarine commercial oyster species, Crassostrea hongkongensis. The primary aim of this study is to understand the influence of DNA methylation over gene expression of mantle tissue under decreased ~pH 7.4, a proxy of OA, and to extrapolate if these molecular changes can be observed in the product of biomineralization-the shell. We grew early juvenile C. hongkongensis, under decreased ~pH 7.4 and control ~pH 8.0 over 4.5 months and studied OA-induced DNA methylation and gene expression patterns along with shell properties such as microstructure, crystal orientation and hardness. The population of oysters used in this study was found to be moderately resilient to OA at the end of the experiment. The expression of key biomineralization-related genes such as carbonic anhydrase and alkaline phosphatase remained unaffected; thus, the mechanical properties of the shell (shell growth rate, hardness and crystal orientation) were also maintained without any significant difference between control and OA conditions with signs of severe dissolution. In addition, this study makes three major conclusions: (1) higher expression of Ca binding/signalling-related genes in the mantle plays a key role in maintaining biomineralization under OA; (2) DNA methylation changes occur in response to OA; however, these methylation changes do not directly control gene expression; and (3) OA would be more of a 'dissolution problem' rather than a 'biomineralization problem' for resilient species that maintain calcification rate with normal shell growth and mechanical properties.
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http://dx.doi.org/10.1111/gcb.15675 | DOI Listing |
Sci Adv
March 2025
Shu Chien-Gene Lay Department of Bioengineering, University of California San Diego, La Jolla, CA 92093, USA.
Aortic valve stenosis (AVS) is a progressive disease, wherein males more often develop valve calcification relative to females that develop valve fibrosis. Valvular interstitial cells (VICs) aberrantly activate to myofibroblasts during AVS, driving the fibrotic valve phenotype in females. Myofibroblasts further differentiate into osteoblast-like cells and produce calcium nanoparticles, driving valve calcification in males.
View Article and Find Full Text PDFPLoS One
March 2025
Department of Physics, Khalifa University of Science and Technology, Abu Dhabi, United Arab Emirates.
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March 2025
The Third Clinical Medicine College, Ningxia Medical University (People's Hospital of Ningxia Hui Autonomous Region), Yinchuan, 750002, China.
The activity of Wnt inhibitory factor 1 (WIF1) is reduced upon promoter methylation and is involved in cartilage degradation in osteoarthritis. This study aims to investigate the mechanism by which WIF1 methylation is involved in chondrocyte damage in ankylosing spondylitis (AS). A model of chondrocyte inflammatory injury in AS was constructed by stimulation with interleukin (IL)-17.
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March 2025
Division of Oncology, Department of Medicine I, Medical University of Vienna, Vienna, Austria.
Neuroendocrine tumors (NET) of the lung constitute a rare entity of primary lung malignancies that often exhibit an indolent clinical course. Epigenetics-related differences have been described previously for lung NET, but the clinical significance remains unclear. In this study, we performed genome-wide methylation analysis using the Infinium MethylationEPIC BeadChip technology on FFPE tissues from lung NET treated at two academic centers.
View Article and Find Full Text PDFArch Dermatol Res
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Department of Dermatology, The First Affiliated Hospital of Harbin Medical University, 23 Post Street, Nangang District, Harbin, Heilongjiang, 150001, China.
Long non-coding RNA (lncRNA) TINCR has been shown to play a crucial regulatory role in various tumors. However, its specific mechanism of action in cutaneous squamous cell carcinoma (CSCC) remains unclear. This study aimed to explore the role of lncRNA TINCR in CSCC.
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