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The systematics of the family Dendrodorididae, with only three valid genera, is a challenge for integrative taxonomists. Its members lack hard structures for morphological comparisons and their mitochondrial and nuclear markers provide contradictory phylogenetic signals, making phylogenetic reconstructions difficult. This molecular discordance has been hypothesized to be the result of nuclear pseudogenes or exogenous contamination. However, these hypotheses have not been tested. Here, we assembled the first genome drafts of seven Dendrodorididae species to investigate the evolutionary processes of this family. Two of the mitogenomes displayed an identical structural rearrangement involving the translocation of three coding genes and five tRNAs, described for the first time in nudibranchs. In addition, we found particularly high dN and dN/dS values and multiple insertions and deletions on the mitochondrial genes of smooth Dendrodoris. In contrast, nuclear single-copy ortholog genes showed no such mutational differences. Models of protein structures from mitochondrial genes are conserved, suggesting conserved functionality. Phylogenies using mitogenomic and nuclear data showed that species with rearranged mitogenomes form a clade, although Dendrodorididae relationships remained unresolved. The present study provides novel evidence for accelerated mutation rates in the mitogenomes of Dendrodorididae, which presumably have implications on respiratory adaptation, and highlights the importance of using genomic data to unveil rare evolutionary processes, crucial for correctly inferring phylogenies.
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http://dx.doi.org/10.1016/j.ympev.2024.108218 | DOI Listing |
Future Med Chem
September 2025
Institute of Bioinformatics and Medical Engineering, School of Electrical and Information Engineering, Jiangsu University of Technology, Changzhou, P.R. China.
The nuclear receptor binding SET domain (NSD) family of histone methyltransferases, which comprised NSD1, NSD2, and NSD3. They play a pivotal role in catalyzing mono- and dimethylation of histone H3 at lysine 36 (H3K36me1/2), a modification critical for maintaining chromatin structure and transcriptional fidelity. Dysregulation of NSD enzymes, often through overexpression, mutation, or chromosomal translocation, has been implicated in a broad spectrum of malignancies and various diseases.
View Article and Find Full Text PDFStem Cell Rev Rep
September 2025
Stem Cells and Metabolism Research Program (STEMM), Research Programs Unit, Faculty of Medicine, University of Helsinki, Helsinki, 00014, Finland.
Mutations in Delta Like Non-Canonical Notch Ligand 1 (DLK1), a paternally expressed imprinted gene, underlie central precocious puberty (CPP), yet the mechanism remains unclear. To test the hypothesis that DLK1 plays a role in gonadotropin releasing hormone (GnRH) neuron ontogeny, 75 base pairs were deleted in both alleles of DLK1 exon 3 with CRISPR-Cas9 in human pluripotent stem cells (hPSCs). This line, exhibiting More than 80% loss of DLK1 protein, was differentiated into GnRH neurons by dual SMAD inhibition (dSMADi), FGF8 treatment and Notch inhibition, as previously described, however, it did not exhibit accelerated GNRH1 expression.
View Article and Find Full Text PDFMedicine (Baltimore)
September 2025
Department of Pediatrics, Affiliated Hospital of Jining Medical University, Jining, Shandong Province, China.
Rationale: Weaver syndrome is a rare congenital overgrowth disorder characterized by a wide spectrum of clinical manifestations that often overlap with other overgrowth syndromes. It is primarily caused by pathogenic variants in the Enhancer of Zeste Homolog 2 (EZH2) gene on chromosome 7q36.1.
View Article and Find Full Text PDFSci China Life Sci
September 2025
The Key Laboratory of Cell Proliferation and Differentiation of the Ministry of Education, College of Life Sciences, Peking University, Beijing, 100871, China.
Hutchinson-Gilford progeria syndrome (HGPS) is a rare progeroid disorder, and approximately 90% of cases are caused by LMNA mutation that yields the lamin A/C variant progerin. Progerin is toxic, and its clearance and disruption have positive benefits on HGPS cells and mice and even HGPS patients. However, accelerating progerin clearance is still an unaddressed issue.
View Article and Find Full Text PDFJ Chem Inf Model
September 2025
College of Agriculture and Biological Science, Dali University, Dali 671000, China.
The E76K mutation in protein tyrosine phosphatase (PTP) SHP2 is a recurrent driver of developmental disorders and cancers, yet the mechanism by which this single-site substitution promotes persistent activation remains elusive. Here, we combine path-based conformational sampling, unbiased molecular dynamics (MD) simulations, Markov state models (MSMs), and neural relational inference (NRI) to elucidate how E76K reshapes the activation landscape and regulatory architecture of SHP2. Using a minimum-action trajectory derived from experimentally determined closed and open structures, we generated representative transition intermediates to guide the unbiased MD simulations.
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