98%
921
2 minutes
20
Admixture resulting from natural dispersal processes can potentially generate novel phenotypic variation that may facilitate persistence in changing environments or result in the loss of population-specific adaptations. Yet, under the US Endangered Species Act, policy is limited for management of individuals whose ancestry includes a protected taxon; therefore, they are generally not protected under the Act. This issue is exemplified by the recently re-established grey wolves of the Pacific Northwest states of Washington and Oregon, USA. This population was likely founded by two phenotypically and genetically distinct wolf ecotypes: Northern Rocky Mountain (NRM) forest and coastal rainforest. The latter is considered potentially threatened in southeast Alaska and thus the source of migrants may affect plans for their protection. To assess the genetic source of the re-established population, we sequenced a ~ 300 bp portion of the mitochondrial control region and ~ 5 Mbp of the nuclear genome. Genetic analysis revealed that the Washington wolves share ancestry with both wolf ecotypes, whereas the Oregon population shares ancestry with NRM forest wolves only. Using ecological niche modelling, we found that the Pacific Northwest states contain environments suitable for each ecotype, with wolf packs established in both environmental types. Continued migration from coastal rainforest and NRM forest source populations may increase the genetic diversity of the Pacific Northwest population. However, this admixed population challenges traditional management regimes given that admixture occurs between an adaptively distinct ecotype and a more abundant reintroduced interior form. Our results emphasize the need for a more precise US policy to address the general problem of admixture in the management of endangered species, subspecies, and distinct population segments.
Download full-text PDF |
Source |
---|---|
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6327037 | PMC |
http://dx.doi.org/10.1038/s41437-018-0094-x | DOI Listing |
J Clin Invest
September 2025
The University of Texas at Austin, Austin, United States of America.
Background: Following SARS-CoV-2 infection, ~10-35% of COVID-19 patients experience long COVID (LC), in which debilitating symptoms persist for at least three months. Elucidating biologic underpinnings of LC could identify therapeutic opportunities.
Methods: We utilized machine learning methods on biologic analytes provided over 12-months after hospital discharge from >500 COVID-19 patients in the IMPACC cohort to identify a multi-omics "recovery factor", trained on patient-reported physical function survey scores.
J Neurooncol
September 2025
Department of Neurological Surgery, Northwestern University Feinberg School of Medicine, Chicago, IL, USA.
Purpose: NOTCH3 is increasingly implicated for its oncogenic role in many malignancies, including meningiomas. While prior work has linked NOTCH3 expression to higher-grade meningiomas and treatment resistance, the metabolic phenotype of NOTCH3 activation remains unexplored in meningioma.
Methods: We performed single-cell RNA sequencing on NOTCH3 + human meningioma cell lines.
Pediatr Crit Care Med
September 2025
Department of Anesthesiology and Critical Care, Children's Hospital of Philadelphia and University of Pennsylvania Perelman School of Medicine, Philadelphia, PA.
Objective: To develop a set of pediatric neurocritical care (PNCC) entrustable professional activities (EPAs) for pediatric critical care medicine (PCCM).
Design: Survey and Delphi methodology in a panel of experts from the Pediatric Neurocritical Care Research Group (PNCRG) and the Education in Pediatric Intensive Care (EPIC) Research Collaborative.
Setting: Interprofessional local focus group, national focus group, and subsequent national multi-institutional, multidisciplinary expert panel in the United States.
Nucleic Acids Res
September 2025
Department of Molecular Biosciences, Northwestern University, Evanston, IL 60208, United States.
DDX6 is known to repress messenger RNA (mRNA) translation and promote mRNA decay in microRNA-mediated silencing. In embryonic stem cells (ESCs), DDX6 primarily functions at the translation level, independent of mRNA destabilization; however, the precise molecular mechanism of how DDX6 represses translation remains unclear. Here, we identify DDX3X as a key downstream target of DDX6-mediated translational repression in ESCs.
View Article and Find Full Text PDF