Abstract
SCIENCE SIGNALING Glutamate mediates functions such as synaptic plasticity, proliferation, and survival via metabotropic receptors (mGluRs) on neurons and glial cells. Sitcheran et al . demonstrate that glutamate promotes the binding of the p65 and p50 subunits of the transcription factor NF-κB to DNA. Glutamate activation of NF-κB was comparable to that produced by epidermal growth factor (EGF) binding to its receptor EGFR, which is found on astrocytes. Glutamate also induced the phosphorylation and activation of inhibitor of κB kinase α and β (IKKα and IKKβ) and of p65. In canonical NF-κB signaling, IKKβ phosphorylates IκBα, which leads to its degradation and the release of active NF-κB subunits, but glutamate did not increase phosphorylation or degradation of IκBα, although it did dissociate IκBα and p65. Knockdown of EGFR blocked mGluR5-stimulated phosphorylation of p65; conversely, mGluR5 stimulation led to the phosphorylation of tyrosine residues in EGFR and to its association with mGluR5. A Ca2+ chelator blocked mGluR5-mediated NF-κB activation, and an inhibitor of EGFR activity reduced mGluR5-stimulated Ca2+ signaling. Together, these data suggest that EGFR signaling is critical for the activation of NF-κB by glutamate. — JFF Mol. Cell. Biol. 28 , 5061 (2008).
Highlights
Lotteries have become a widespread means of generating billions of dollars for state treasuries in the United States
Maurer et al have used cryoelectron tomography to reconstruct three-dimensional images of herpes simplex virus type 1 (HSV-1) particles frozen in the process of entering kidney cells and synaptic nerve endings
HSV-1 particles consist of a glycoprotein-rich outer membrane surrounding an amorphous protein layer and an icosahedral capsid housing the DNA genome
Summary
Ionizing radiation is harmful to living creatures because it scythes through both strands of genomic DNA, leading to potentially lethal chromosome aberrations. To identify the origin of these aberrations, Argueso et al have used x-rays to shred the genomes of diploid yeast cells and introduced a staggering ~250 DNA breaks per cell; within 3 hours, most of the shattered chromosomes had been stitched together, with half of the analyzed surviving cells harboring at least one chromosome aberration. A molecular autopsy revealed that most aberrations were associated with a repetitive sequence, the Ty retrotransposon, a selfish DNA element scattered throughout the yeast genome, and that the aberrations appeared to have arisen via failed DNA repair attempts. For breaks that occur in or near Ty elements, rather than the homologous element being used, any of the Ty elements in the yeast genome might be selected, mixing chromosomal material and making repetitive DNA a driving force for genomic variation.
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