Mutations in the BREVIPEDICELLUS (BP) gene of Arabidopsis thaliana condition a pleiotropic phenotype featuring defects in internode elongation, the homeotic conversion of internode to node tissue, and downward pointing flowers and pedicels. We have characterized five mutant alleles of BP, generated by EMS, fast neutrons, x-rays, and aberrant T-DNA insertion events. Curiously, all of these mutagens resulted in large deletions that range from 140 kbp to over 900 kbp just south of the centromere of chromosome 4. The breakpoints of these mutants were identified by employing inverse PCR and DNA sequencing. The south breakpoints of all alleles cluster in BAC T12G13, while the north breakpoint locations are scattered. With the exception of a microhomology at the bp-5 breakpoint, there is no homology in the junction regions, suggesting that double-stranded breaks are repaired via non-homologous end joining. Southwestern blotting demonstrated the presence of nuclear matrix binding sites in the south breakpoint cluster (SBC), which is A/T rich and possesses a variety of repeat sequences. In situ hybridization on pachytene chromosome spreads complemented the molecular analyses and revealed heretofore unrecognized structural variation between the Columbia and Landsberg erecta genomes. Data mining was employed to localize other large deletions around the HY4 locus to the SBC region and to show that chromatin modifications in the region shift from a heterochromatic to euchromatic profile. Comparisons between the BP/HY4 regions of A. lyrata and A. thaliana revealed that several chromosome rearrangement events have occurred during the evolution of these two genomes. Collectively, the features of the region are strikingly similar to the features of characterized metazoan chromosome fragile sites, some of which are associated with karyotype evolution.
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http://dx.doi.org/10.1371/journal.pgen.1003136 | DOI Listing |
Int J Mol Sci
January 2025
Department of Women's and Children's Health, University of Padova, 35128 Padova, Italy.
Fragile X syndrome (FXS) is a genetic neurodevelopmental disorder that causes a range of developmental problems including cognitive and behavioral impairment and learning disabilities. FXS is caused by full mutations (FM) of the gene expansions to over 200 repeats, with hypermethylation of the cytosine-guanine-guanine (CGG) tandem repeated region in its promoter, resulting in transcriptional silencing and loss of gene function. Female carriers of FM are typically less impaired than males.
View Article and Find Full Text PDFSci Rep
January 2025
Biology School, University of Costa Rica, San Pedro, San José, 11501-20260, Costa Rica.
Plasmids play a crucial role in facilitating genetic exchange and enhancing the adaptability of microbial communities. Despite their importance, environmental plasmids remain understudied, particularly those in fragile and underexplored ecosystems such as the deep-sea. In this paper we implemented a bioinformatics pipeline to study the composition, diversity, and functional attributes of plasmid communities (plasmidome) in 81 deep-sea metagenomes from the Tara and Malaspina expeditions, sampled from the Pacific, Atlantic, and Indian Oceans at depths ranging from 270 to 4005 m.
View Article and Find Full Text PDFMech Ageing Dev
February 2025
Department of Medicine, Academy of Applied Medical and Social Sciences-AMiSNS: Akademia Medycznych I Spolecznych Nauk Stosowanych, 2 Lotnicza Street, Elbląg 82-300, Poland; Department of General Surgery and Surgical Oncology, "Saint Wojciech" Hospital, "Nicolaus Copernicus" Health Center, Jana Pawła II 50, Gdańsk 80-462, Poland.
Aging is a complex process that affects individuals at the molecular, cellular, tissue, and systemic levels, arising from the cumulative effects of damage and reduced repair mechanisms. This process leads to the onset of age-related diseases, including cancer, which exhibits increased incidence with age. Telomeres, the protective caps at chromosome ends, play a crucial role in genome stability and are closely connected with aging and age-related disorders.
View Article and Find Full Text PDFInt J Mol Sci
December 2024
Department of Pediatrics, University of Colorado Anschutz Medical Campus, Aurora, CO 80045, USA.
(Fragile X messenger ribonucleoprotein 1), located on the X-chromosome, encodes the multi-functional FMR1 protein (FMRP), critical to brain development and function. Trinucleotide CGG repeat expansions at this locus cause a range of neurological disorders, collectively referred to as Fragile X-related conditions. The most well-known of these is Fragile X syndrome, a neurodevelopmental disorder associated with syndromic facial features, autism, intellectual disabilities, and seizures.
View Article and Find Full Text PDFCells
December 2024
Department of Biomedical Sciences, College of Medicine, Florida State University, Tallahassee, FL 32306, USA.
Fragile X Syndrome (FXS) presents with a constellation of phenotypes, including trouble regulating emotion and aggressive behaviors, disordered sleep, intellectual impairments, and atypical physical development. Genetic study of the X chromosome revealed that substantial repeat expansion of the 5' end of the gene fragile X messenger ribonucleoprotein 1 () promoted DNA methylation and, consequently, silenced expression of . Further analysis proved that shorter repeat expansions in also manifested in disease at later stages in life.
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