Modulation of gene expression through RNA interference is well conserved in eukaryotes and is involved in many cellular processes. In the oomycete , research on the small RNA machinery and function has started to reveal potential roles in the pathogen, but much is still unknown. We examined Argonaute (AGO) homologs within oomycete genome sequences, especially among species, to gain a clearer understanding of the evolution of this well-conserved protein family. We identified AGO homologs across many representative oomycete and stramenopile species, and annotated representative homologs in . Furthermore, we demonstrate variable transcript levels of all identified homologs in comparison to previously identified Dicer-like (DCL) and RNA-dependent RNA polymerase (RDR) homologs. Our phylogenetic analysis further refines the relationship of the AGO homologs in oomycetes and identifies a conserved tandem duplication of homologs in a subset of species.
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http://dx.doi.org/10.3389/fmicb.2018.02841 | DOI Listing |
J Neural Transm (Vienna)
January 2025
Institut für Zellbiochemie, OE 4310, Medizinische Hochschule Hannover, 30623, Hannover, Germany.
Botulinum neurotoxins (BoNT) are established biopharmaceuticals for neuromuscular and secretory conditions based on their ability to block neurotransmitter release from neurons by proteolyzing specific soluble N-ethylmaleimide-sensitive factor attachment protein receptor (SNARE) proteins. Recently, a mutant catalytic domain of serotype E (LC/E) exhibiting 16 mutations was reported to cleave the phosphatase and tensin homolog (PTEN). This molecule represents an attractive new target in neurons as several reports support PTEN knockdown as a strategy to stimulate axonal regeneration after injury.
View Article and Find Full Text PDFMol Biol Evol
January 2025
Swiss Institute of Bioinformatics, Basel, Switzerland.
Bacterial genomes primarily diversify via gain, loss, and rearrangement of genetic material in their flexible accessory genome. Yet the dynamics of accessory genome evolution are very poorly understood, in contrast to the core genome where diversification is readily described by mutations and homologous recombination. Here, we tackle this problem for the case of very closely related genomes.
View Article and Find Full Text PDFEur J Cancer
December 2024
Division of Digital Prevention, Diagnostics and Therapy Guidance, German Cancer Research Center (DKFZ), Heidelberg, Germany. Electronic address:
Fam Cancer
December 2024
Leeds Institute of Medical Research, University of Leeds, Leeds, UK.
Lynch syndrome (LS) is an autosomal dominant hereditary cancer predisposition syndrome whereby the lifetime risk of developing gastrointestinal and genitourinary cancers rises by to over 50%. It is caused by heterozygous variants in the DNA mismatch repair genes- MLH1, MSH2, MSH6 and PMS2, with the majority detected in MLH1 and MSH2. Recurrently observed LS-associated variants in apparently unrelated individuals have either arisen de novo in different families due to mutation hotspots or are inherited from a common ancestor (founder) that lived several generations back.
View Article and Find Full Text PDFGynecol Oncol
January 2025
Gynecologic Medical Oncology Service, Department of Medicine, Memorial Sloan Kettering Cancer Center, New York, NY, USA; Department of Medicine, Weill Cornell Medical College, New York, NY, USA. Electronic address:
Objective: We sought to describe the association between genomic instability score (GIS) and progression-free survival (PFS) and overall survival (OS) in patients with newly diagnosed, non-BRCA1/2 ovarian cancer.
Methods: Homologous recombinant deficiency (HRD) status was based on a cutoff of ≥42 GIS; patients <42 were categorized with homologous recombination proficiency (HRP). We collected type and duration of maintenance therapy, among other variables, and built a multivariate model with landmark analysis at 6 months from baseline and applied it for time-dependent variables.
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