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and , the only two human pathogens of , are closely related species. But the niches they survived in and their pathogenic characteristics are distinctly different. However, the genetic basis of these differences has not yet been fully elucidated. In this study, comparative genomics analysis was performed based on 15 , 75 , and 7 nonpathogenic genomes. Core-pangenome analysis found 1111 conserved gene families among them, and each of these species groups had opening pangenome. We found that 452, 78, and 319 gene families were unique in , , and both of them, respectively. Those unique gene families were regarded as candidates that related to their pathogenicity and niche adaptation. The relationships among them have been partly verified by functional annotation analysis. But at least one-third genes for each gene set have not found the certain functional information. Simple sequence repeat (SSR), the basis of gene phase variation, was found abundant in the membrane or related genes of each unique gene set, which may facilitate their adaptation to variable host environments. Protein-protein interaction (PPI) analysis found at least five distinct PPI clusters in and four in , and 167 and 52 proteins with unknown function were contained within them, respectively.
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http://dx.doi.org/10.1155/2019/6015730 | DOI Listing |
Genes Brain Behav
October 2025
Department of Pharmaceutical Sciences, College of Pharmacy, University of Arkansas for Medical Sciences, Little Rock, Arkansas, USA.
Major depressive disorder is a prevalent and debilitating psychiatric illness that produces significant disability. Clinical data suggest that the pathophysiology of depression is due, in part, to a dysregulation of inflammation and glutamate levels in the brain. The systemic administration of lipopolysaccharide (LPS) has been shown to induce depressive-like behaviors in mice.
View Article and Find Full Text PDFHGG Adv
September 2025
Department of Medicine IV, Faculty of Medicine, Medical Center-University of Freiburg, University of Freiburg, Freiburg, Germany; Medizinische Genetik Mainz, Limbach Genetics, Mainz, Germany. Electronic address:
Cystic kidney disease and related ciliopathies are caused by pathogenic variants in genes that commonly result in ciliary dysfunction. For a substantial number of individuals affected by those cilia-related diseases, the causative gene still remains unknown. Using massively parallel sequencing, we here identified a pathogenic bi-allelic variant in the gene encoding PALS1-Associated Tight Junction Protein (PATJ; also known as Inactivation-No-Afterpotential D-Like, INADL) in an individual with ciliopathy.
View Article and Find Full Text PDFActa Neuropathol Commun
September 2025
Department of Biomedical and Clinical Sciences and Department of Clinical Pathology, Linköping University, 58185, Linköping, Sweden.
Disruptions in synaptic transmission and plasticity are early hallmarks of Alzheimer's disease (AD). Endosomal trafficking, mediated by the retromer complex, is essential for intracellular protein sorting, including the regulation of amyloid precursor protein (APP) processing. The VPS35 subunit, a key cargo-recognition component of the retromer, has been implicated in neurodegenerative diseases, with mutations such as L625P linked to early-onset AD.
View Article and Find Full Text PDFExp Appl Acarol
September 2025
Institute of Pathogens and Vectors, Yunnan Provincial Key Laboratory for Zoonosis Control and Prevention, Dali University, 22 Wanhua St, Dali, 671000, China.
The family Spinturnicidae belongs to the suborder Monogynapsida, superfamily Dermanyssoidea, and exclusively parasitizes the body surface of bats. In the present study, we determined the complete mitochondrial genome of Spinturnix psi, a species of bat mite, and subsequently conducted a comprehensive analysis of its genomic information. The mitochondrial genome of S.
View Article and Find Full Text PDFMol Syst Biol
September 2025
Department of Medicine, Division of Cardiovascular Medicine, Stanford University, Stanford, CA, USA.
Vascular sites have distinct susceptibility to atherosclerosis and aneurysm, yet the epigenomic and transcriptomic underpinning of vascular site-specific disease risk is largely unknown. Here, we performed single-cell chromatin accessibility (scATACseq) and gene expression profiling (scRNAseq) of mouse vascular tissue from three vascular sites. Through interrogation of epigenomic enhancers and gene regulatory networks, we discovered key regulatory enhancers to not only be cell type, but vascular site-specific.
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