Publications by authors named "Amy Meltzer"

Whole-genome duplication (WGD) is a frequent event in cancer evolution that fuels chromosomal instability. WGD can result from mitotic errors or endoreduplication, yet the molecular mechanisms that drive WGD remain unclear. Here, we use live single-cell analysis to characterize cell-cycle dynamics upon aberrant Ras-ERK signaling.

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Whitebark pine (WBP, Pinus albicaulis) is a white pine of subalpine regions in the Western contiguous United States and Canada. WBP has become critically threatened throughout a significant part of its natural range due to mortality from the introduced fungal pathogen white pine blister rust (WPBR, Cronartium ribicola) and additional threats from mountain pine beetle (Dendroctonus ponderosae), wildfire, and maladaptation due to changing climate. Vast acreages of WBP have suffered nearly complete mortality.

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Article Synopsis
  • Whitebark pine (WBP) is under threat from disease like white pine blister rust, pests, wildfires, and climate change, leading to severe mortality across its range in the Western US and Canada.
  • Genomic technologies have been utilized to effectively identify disease-resistant and climate-adapted seed sources for restoring WBP, including advanced sequencing techniques that produced a detailed genome assembly.
  • The study identified a significant number of candidate genes for disease resistance, particularly focusing on nucleotide-binding leucine-rich-repeat receptors (NLRs), enhancing the ability to understand and improve WBP’s resilience compared to earlier methods.
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Purpose Although children with hearing loss (HL) can benefit from cochlear implants (CIs) and hearing aids (HAs), they often show language delays. Moreover, little is known about the mechanisms by which children with HL learn words. One mechanism by which typically hearing (TH) children learn words is by acquiring word learning biases such as the "shape bias," that is, generalizing the names of novel solid objects by similarity in shape.

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There have been no reports describing the effects of cancer cell-derived extracellular vesicles (EVs) on three-dimensional organoids. In this study, we delineated the proneoplastic effects of esophageal adenocarcinoma (EAC)-derived EVs on gastric organoids (gastroids) and elucidated molecular mechanisms underlying these effects. EVs were identified using PKH-67 staining.

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