The wide usage of neodymium (Nd) in industry, agriculture, and medicine has made it become an emerging pollutant in the environment. Increasing Nd pollution has potential hazards to plants, animals, and microorganisms. Thus, it is necessary to study the toxicity of Nd and the mechanism of Nd transportation and detoxification in microorganisms. Through genome-scale screening, we identified 70 yeast monogene deletion mutations sensitive to Nd ions. These genes are mainly involved in metabolism, transcription, protein synthesis, cell cycle, DNA processing, protein folding, modification, and cell transport processes. Furthermore, the regulatory networks of Nd toxicity were identified by using the protein interaction group analysis. These networks are associated with various signal pathways, including calcium ion transport, phosphate pathways, vesicular transport, and cell autophagy. In addition, the content of Nd ions in yeast was detected by an inductively coupled plasma mass spectrometry, and most of these Nd-sensitive mutants showed an increased intracellular Nd content. In all, our results provide the basis for understanding the molecular mechanisms of detoxifying Nd ions in yeast cells, which will be useful for future studies on Nd-related issues in the environment, agriculture, and human health.
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http://dx.doi.org/10.1007/s11356-021-18100-2 | DOI Listing |
Mol Ther
January 2025
Department CIBIO, University of Trento, Via delle Regole 101, 38123 Trento, Italy. Electronic address:
Cystic Fibrosis (CF) is a life-shortening autosomal recessive disease caused by mutations in the CFTR gene, resulting in functional impairment of the encoded ion channel. F508del mutation, a trinucleotide deletion, is the most frequent cause of CF affecting approximately 80% of persons with cystic fibrosis (pwCFs). Even though current pharmacological treatments alleviate the F508del-CF disease symptoms there is no definitive cure.
View Article and Find Full Text PDFInt J Mol Sci
December 2024
College of Resources and Environment, Fujian Agriculture and Forestry University, Fuzhou 350002, China.
Microbes have been shown to adapt to stressful or even lethal conditions through displaying genome plasticity. However, how bacteria utilize the ability of genomic plasticity to deal with high antimony (Sb) stress has remained unclear. In this study, the spontaneous mutant strain SMAs-55 of sp.
View Article and Find Full Text PDFTaiwan J Obstet Gynecol
January 2025
Department of Obstetrics and Gynecology, Changhua Christan Hospital, Changhua, Taiwan. Electronic address:
Objective: Prenatal diagnosis of fetal 13q34 microdeletion is a rare condition, which may present with abnormal fetal development, including facial dysmorphism, mental retardation, and developmental delay. We present a pregnant woman in whom the fetus presented with a 0.24-cm ventricular septal defect at 20 weeks of gestation, with fetal 13q34 (113610612-115092648) deletion.
View Article and Find Full Text PDFStem Cell Res
December 2024
Division of Medical Genetics and Metabolism, Department of Pediatrics, Pusan National University School of Medicine, Pusan National University Children's Hospital, Yangsan 50612, Gyeongsangnam-do, Republic of Korea. Electronic address:
Mucopolysaccharidosis Type Ⅱ, as Known as Hunter syndrome, is a rare X-liked genetic disease caused by mutations in iduronate-2-sulfatase (IDS) gene. We obtained peripheral blood mononuclear cells (PBMCs) from a patient with a severe type of Hunter syndrome carrying c.418 + 495_1006 + 1304 deletion in the IDS gene.
View Article and Find Full Text PDFProc Natl Acad Sci U S A
January 2025
Center for Nutritional Sciences, Food Science and Human Nutrition Department, College of Agricultural and Life Sciences, University of Florida, Gainesville, FL 32611.
Documented worldwide, impaired immunity is a cardinal signature resulting from loss of dietary zinc, an essential micronutrient. A steady supply of zinc to meet cellular requirements is regulated by an array of zinc transporters. Deletion of the transporter Zip14 (Slc39a14) in mice produced intestinal inflammation.
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