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Kallio, K.

Publications and source records attributed to Kallio, K..

3 recordsLinked to original sources

Structure and signaling mechanism of Helicobacter pylori transducer-like protein D

Chemoreceptors, or methyl-accepting chemotaxis proteins (MCPs), are ancient and widespread prokaryotic sensors that direct taxis in response to stimuli and are attractive targets for therapeutic control of bacteria 1-4. Decades of study have yielded substantial mechanistic insight into chemoreceptor function, but the absence of high-resolution full-length structures containing ligand-binding domains (LBD) has limited understanding of how effector sensing is structurally coupled to long-range signal transduction. Here, we present the intact structure of the chemoreceptor transducer-like protein D (TlpD) from the gastric pathogen Helicobacter pylori, in complex with its ligand Zn2+, determined by X-ray crystallography in two crystal forms at 2.4-3.0 [A]. Three different conformations are captured, revealing how interactions in the ligand-binding site of the chemoreceptor zinc-binding (CZB) domain are interconnected with the distal kinase interface. Small changes at the ligand-binding site coincide with cascades of side-chain rearrangements across the dimer, distortion of the receptor coiled-coil, and conformational and dynamic shifts at the kinase interface over 140 [A] away. These near-atomic resolution structures provide a framework for understanding cooperativity and allosteric communication in chemoreceptors, and establish a representative model for a widespread class of soluble chemoreceptors important in bacterial pathogenesis 2,5.

molecular biology↗

A microbiota membrane disrupter disseminates to the pancreas and increases β-cell mass

Microbiome dysbiosis is a feature of diabetes, but how microbial products influence insulin production is poorly understood. Here we report the mechanism of BefA, a microbiome-derived protein that increases proliferation of insulin-producing {beta}-cells during pancreatic development in gnotobiotic zebrafish and mice. BefA disseminates systemically via multiple anatomic routes to act directly on pancreatic islets. We report the structure of BefA, containing a lipid-binding SYLF domain, and demonstrate that it permeabilizes synthetic liposomes and bacterial membranes. A BefA mutant impaired in membrane disruption fails to expand {beta}-cells whereas the pore-forming host defense protein, Reg3, stimulates {beta}-cell proliferation. Our work demonstrates that membrane permeabilization by microbiome-derived and host defense proteins is necessary and sufficient for {beta}-cell expansion during pancreas development, thereby connecting microbiome composition with diabetes risk.

molecular biology↗

Neuropilin-1 facilitates SARS-CoV-2 cell entry and provides a possible pathway into the central nervous system

The causative agent of the current pandemic and coronavirus disease 2019 (COVID-19) is the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)1. Understanding how SARS-CoV-2 enters and spreads within human organs is crucial for developing strategies to prevent viral dissemination. For many viruses, tissue tropism is determined by the availability of virus receptors on the surface of host cells2. Both SARS-CoV and SARS-CoV-2 use angiotensin-converting enzyme 2 (ACE2) as a host receptor, yet, their tropisms differ3-5. Here, we found that the cellular receptor neuropilin-1 (NRP1), known to bind furin-cleaved substrates, significantly potentiates SARS-CoV-2 infectivity, which was inhibited by a monoclonal blocking antibody against the extracellular b1b2 domain of NRP1. NRP1 is abundantly expressed in the respiratory and olfactory epithelium, with highest expression in endothelial cells and in the epithelial cells facing the nasal cavity. Neuropathological analysis of human COVID-19 autopsies revealed SARS-CoV-2 infected NRP1-positive cells in the olfactory epithelium and bulb. In the olfactory bulb infection was detected particularly within NRP1-positive endothelial cells of small capillaries and medium-sized vessels. Studies in mice demonstrated, after intranasal application, NRP1-mediated transport of virus-sized particles into the central nervous system. Thus, NRP1 could explain the enhanced tropism and spreading of SARS-CoV-2.

microbiology↗