The presence of L-rhamnose (Rha) branches in the coaggregation receptor polysaccharides (RPS) of Streptococcus gordonii 38 and Streptococcus oralis J22 was eliminated by replacement of wefB with ermAM in these strains. The expression of this gene in S. oralis 34 did not, however, result in the addition of Rha branches to the linear RPS of this strain, which is identical to that produced by the wefB-deficient mutant of S. gordonii 38. This paradoxical finding was explained by a subtle difference in acceptor specificity of the galactose-1-phosphotransferases encoded by downstream wefC in S. gordonii 38 and wefH in S. oralis 34. These genes were distinguished by the unique ability of WefC to act on the branched acceptor formed by the action of WefB.
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http://dx.doi.org/10.1128/JB.01843-05 | DOI Listing |
Elife
November 2024
Cellular Informatics Laboratory, RIKEN Cluster for Pioneering Research, Wako, Japan.
Anionic lipid molecules, including phosphatidylinositol-4,5-bisphosphate (PI(4,5)P), are implicated in the regulation of epidermal growth factor receptor (EGFR). However, the role of the spatiotemporal dynamics of PI(4,5)P in the regulation of EGFR activity in living cells is not fully understood, as it is difficult to visualize the local lipid domains around EGFR. Here, we visualized both EGFR and PI(4,5)P nanodomains in the plasma membrane of HeLa cells using super-resolution single-molecule microscopy.
View Article and Find Full Text PDFProc Natl Acad Sci U S A
June 2024
Department of Biochemistry and Molecular Biology, Colorado State University, Fort Collins, CO 80523.
Synapses containing γ-aminobutyric acid (GABA) constitute the primary centers for inhibitory neurotransmission in our nervous system. It is unclear how these synaptic structures form and align their postsynaptic machineries with presynaptic terminals. Here, we monitored the cellular distribution of several GABAergic postsynaptic proteins in a purely glutamatergic neuronal culture derived from human stem cells, which virtually lacks any vesicular GABA release.
View Article and Find Full Text PDFCommun Biol
March 2024
Weinberg ALS Center, Vickie and Jack Farber Institute for Neuroscience, Department of Neuroscience, Thomas Jefferson University, Philadelphia, PA, USA.
Expanded intronic GC repeats in the C9ORF72 gene cause amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD). These intronic repeats are translated through a non-AUG-dependent mechanism into five different dipeptide repeat proteins (DPRs), including poly-glycine-arginine (GR), which is aggregation-prone and neurotoxic. Here, we report that Kapβ2 and GR interact, co-aggregating, in cultured neurons in-vitro and CNS tissue in-vivo.
View Article and Find Full Text PDFJ Clin Invest
February 2024
Université Paris Cité, Institute of Psychiatry and Neuroscience of Paris (IPNP), INSERM U1266, Paris, France.
Loss of arterial smooth muscle cells (SMCs) and abnormal accumulation of the extracellular domain of the NOTCH3 receptor (Notch3ECD) are the 2 core features of CADASIL, a common cerebral small vessel disease caused by highly stereotyped dominant mutations in NOTCH3. Yet the relationship between NOTCH3 receptor activity, Notch3ECD accumulation, and arterial SMC loss has remained elusive, hampering the development of disease-modifying therapies. Using dedicated histopathological and multiscale imaging modalities, we could detect and quantify previously undetectable CADASIL-driven arterial SMC loss in the CNS of mice expressing the archetypal Arg169Cys mutation.
View Article and Find Full Text PDFAdv Healthc Mater
April 2024
Biionix Cluster, University of Central Florida, Orlando, FL, 32827, USA.
Periprosthetic joint infection (PJI) is a challenging complication that can occur following joint replacement surgery. Efficacious strategies to prevent and treat PJI and its recurrence remain elusive. Commensal bacteria within the gut convey beneficial effects through a defense strategy named "colonization resistance" thereby preventing pathogenic infection along the intestinal surface.
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