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Mansfield, B.

Publications and source records attributed to Mansfield, B..

2 recordsLinked to original sources

A novel genetically distinct Amdoparvovirus in Sorex araneus in the United Kingdom highlights an unexplored ancestral link

Amdoparvoviruses have historically been documented almost exclusively in carnivores, with recent detections in bats. However, endogenous viral elements in rodent genomes suggest a more ancient and taxonomically broader evolutionary history. Despite this, small mammals have never been systematically surveyed for extant amdoparvovirus infections. In this study, we used whole genome sequencing to screen four different shrew species and wild American mink in the UK, which may act as a reservoir host for amdoparvoviruses. We identified a highly divergent amdoparvovirus in native common shrews (Sorex araneus) from northern England, tentatively named Shrew parvovirus 1(SP 1). Classical amdoparvovirus sequences were also detected in wild American mink (Neogale vison), confirming the presence of known amdoparvovirus strains in UK mustelids. Phylogenetic analysis revealed that the shrew virus, SP 1, forms a distinct clade, suggesting ancient divergence or long-term cryptic circulation in small mammal reservoirs. These findings fundamentally challenge the hypothesis that amdoparvoviruses are carnivore-restricted pathogens and underscore the importance of systematic wildlife surveillance for understanding viral host range evolution and assessing spillover risks.

evolutionary biology↗

An Nlrp5-null mutation leads to attenuated de novo methylation in oocytes, accompanied by a significant reduction in DNMT3L

Nlrp5 encodes a core component of the subcortical maternal complex (SCMC) a cytoplasmic protein structure unique to the mammalian oocyte and cleavage-stage embryo. NLRP5 mutations have been identified in patients presenting with early embryo arrest, recurrent molar pregnancies and imprinting disorders. Correct patterning of DNA methylation over imprinted domains during oogenesis is necessary for faithful imprinting of genes. It was previously shown that oocytes with mutation in the human SCMC gene KHDC3L had globally impaired methylation, indicating that integrity of the SCMC is essential for correct establishment of DNA methylation at imprinted regions. Here, we present a multi-omic analysis of an Nlrp5- null mouse model, which in GV oocytes displays a misregulation of a broad range of maternal proteins, including proteins involved in several key developmental processes. This misregulation likely underlies impaired oocyte developmental competence. Amongst impacted proteins are several epigenetic modifiers, including a substantial reduction in DNMT3L; we show that de novo DNA methylation is attenuated in Nlrp5-null oocytes. This provides evidence for mechanisms leading to downstream misregulation of imprinted genes, which in turn, may result in imprinting syndromes, multi-locus imprinting disturbances (MLID) and hydatidiform moles.

developmental biology↗