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Evolutionary simulations of multiple chromosomes, even up to the scale of full-genome simulations, are becoming increasingly important in population genetics and evolutionary ecology. Unfortunately, the popular simulation framework SLiM has always been intrinsically limited to simulations of a single diploid chromosome. Modeling multiple chromosomes of different types, such as sex chromosomes, has always been cumbersome even with scripting, presenting a substantial barrier to the development of full-genome simulations. Here we present SLiM 5, a major extension of SLiM's capabilities for simulating multiple chromosomes. Modeling up to 256 chromosomes is now possible, and each chromosome may belong to any of a wide variety of types - not just autosomes (diploid and haploid), but also sex chromosomes (X, Y, Z, and W), haploid mitochondrial and chloroplast DNA, and more. This new functionality is integrated across all of SLiM, including not only the mechanics of reproduction and inheritance, but also input and output of multi-chromosome data in formats like VCF, and tree-sequence recording across multiple chromosomes. New recipes in the SLiM manual demonstrate these new features, and SLiM's graphical modeling environment, SLiMgui, has been extended in many ways for the visualization of multi-chromosome models. These new features will open new horizons and enable a heightened level of realism for full-genome simulations.
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http://dx.doi.org/10.1101/2025.08.07.669155 | DOI Listing |
Proc Natl Acad Sci U S A
September 2025
Florida Museum of Natural History, University of Florida, Gainesville, FL 32611.
The origin and phylogenetic distribution of symbiotic associations between nodulating angiosperms and nitrogen-fixing bacteria have long intrigued biologists. Recent comparative evolutionary analyses have yielded alternative hypotheses: a multistep pathway of independent gains and losses of root nodule symbiosis vs. a single gain followed by numerous losses.
View Article and Find Full Text PDFBackground: This study aims to gain further insights into the characteristics of the rare subtype of acute myeloid leukemia (AML) with BCR∷ABL by analyzing laboratory detection results of various gene mutations, such as NPM1.
Methods: Laboratory detection results of multiple gene missense mutations, including NPM1, were analyzed in a case of primary AML with BCR∷ABL.
Results: The patient exhibited morphological features of acute leukemia in the bone marrow.
Medicine (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 PDFBiochim Biophys Acta Rev Cancer
September 2025
Department of Hematology, Navy Medical Center of PLA, Naval Medical University, Shanghai 200052, China,. Electronic address:
Clonal hematopoiesis of indeterminate potential (CHIP) bridges hematopoietic clonality and solid tumorigenesis, unveiling a systemic dimension of somatic mutagenesis in cancer biology. Generally, population studies demonstrate CHIP carriers face elevated risks of cancer and poorer survival outcomes. This review consolidates current knowledge on the role of CHIP as potential biomarkers in the prediction/early detection/prognosis evaluation of various non-hematological cancers.
View Article and Find Full Text PDFExp Hematol
September 2025
Tsuruoka Metabolomics Laboratory, National Cancer Center, Tsuruoka, Yamagata 997-0052, Japan. Electronic address:
Gene rearrangements of the human MLL gene (also known as KMT2A) generate multiple fusion oncoproteins which cause leukemia with poor prognosis. MLL is an epigenetic regulator that reads and writes epigenetic information and has an evolutionarily conserved role maintaining expression of Homeotic (HOX) genes during embryonic development. Most MLL gene rearrangements found in leukemia generate a constitutively active version of the wild-type protein, which causes overexpression of HOX and other genes and leukemic transformation of normal hematopoietic progenitors.
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