New publication from the Harris lab: Triggers for Prion toxicity
Prion diseases are fatal neurodegenerative disorders that affect both humans and animals. These diseases are caused by PrPSc, a misfolded and infectious isoform of the normal cellular prion protein (PrPC), which propagates by a self-templating mechanism. While considerable progress has been made in understanding prion propagation and infectivity, the early cellular events that initiate prion-induced synaptic loss and neurodegeneration remain poorly defined.
A recent publication in PLoS Pathogens from the Harris lab, led by graduate student Jean Gatdula, focused on the initial molecular events on the neuronal surface that initiate prion synaptotoxicity. Using a specialized neuronal culture system that allows direct measurements of synaptic integrity, they found that experimental manipulations that blocked formation of pathogenic PrPSc on the neuronal surface prevented synaptic damage. Thus, membrane-attached PrPSc molecules are directly responsible for triggering a prion synaptotoxic signaling cascade, presumably by interacting with other proteins or lipids on the membrane surface. These results not only illuminate basic pathogenic mechanisms, but they suggest a novel therapeutic approach using PrP molecules that are locked in the PrPC conformation.
Congratulations Cheyanne Frosti
Congratulations to Cheyanne Frosti in the Layne lab for successfully defending her PhD dissertion; "MECHANOREGULATION OF FIBROBLAST ACTIVATION BY AORTIC CARBOXYPEPTIDASE-LIKE PROTEIN"
New publication from the Garcia-Marcos Lab: Inhibitory probes for spatiotemporal analysis of Gαs protein signaling
NEW PUBLICATION BY THE GARCIA-MARCOS LAB
A recent publication in Nature Chemical Biology (https://www.nature.com/articles/s41589-025-02138-1) led by Jingyi Zhao in the Garcia-Marcos Lab describes the discovery and optimization of broadly applicable genetically-encoded probes and peptide-based compounds specifically inhibit Gαs, the prototypical signal transducer of G protein-coupled receptors (GPCRs). These tools were leveraged to provide new mechanistic insights into GPCR signaling at the subcellular scale by revealing definitive evidence for G protein signaling at endosomes. The newly developed peptide-based compound named α-sintide allowed the inhibition signaling in multiple contexts: blocking an oncogenic G protein mutant, inhibiting heart cell responses to adrenaline, or preventing T cell exhaustion.
This work was done in collaboration with the Varelas Lab in our Department and with the Irannejad Lab and Vilardaga Lab at UCSF and U of Pittsburgh, respectively.
Congratulations to our BU Pilot Grant Awardees!
Congratulations to our BU Pilot Grant Awardees!
Please join us in congratulating the five Biochemistry & Cell Biology PIs who were selected for BU Pilot Grants:
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Daniel Cifuentes – Spivack Neuroscience Pilot Grant
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Valentina Perissi – Dahod Breast Cancer Research Pilot Grant
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Nelson Lau – Sexual Medicine Pilot Grant
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Bob Varelas – Dahod Breast Cancer Research Pilot Grant
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Mike Blower – Shipley Prostate Cancer Pilot Grant
Well deserved—congratulations to all!
New research from the Cifuentes Lab: RBPscan, a quantitative in vivo tool for profiling RNA-binding protein interactions.
New research from the Cifuentes Lab: RBPscan, a quantitative in vivo tool for profiling RNA-binding protein interactions.
Researchers in the Cifuentes lab at Boston University have published a new study in Molecular Cell describing RBPscan, a method that enables quantitative measurement of protein-RNA interactions directly in living cells.
RNA-binding proteins regulate nearly every step of gene expression, but existing methods have made it difficult to determine where these proteins bind and how strongly they interact with RNA in their native cellular context. RBPscan was developed to address this challenge by combining RNA editing with massively parallel reporter assays to provide a simple, scalable, and quantitative readout of protein-RNA interactions in vivo.
The study demonstrates that RBPscan can identify both linear and structured RNA-binding motifs, quantify relative binding affinities across multiple experimental systems including human cells, zebrafish embryos, and yeast, and link binding strength to functional outcomes such as mRNA decay. The method also enables precise mapping of binding sites within full-length transcripts, providing positional information that complements existing approaches.
By making quantitative analysis of protein-RNA interactions more accessible, RBPscan provides a versatile new tool for studying post-transcriptional gene regulation and opens the door to discovering how RNA-binding proteins function in their native biological contexts.
Congratulations to the exceptional and dedicated Cifuentes lab team who made this work possible, with Dmitry Kretov spearheading the experimental work and now leading his own lab at CHU de Québec-Université Laval Research Center.
Publisher online February 6th, 2026.
Links to the paper:
https://authors.elsevier.com/a/1mZlb3vVUPZNXj
https://www.cell.com/molecular-cell/fulltext/S1097-2765(26)00023-7
New research from the Grishok Lab: spermatogenic Argonaute proteins are activated by Insulin/IGF-1 Signaling and promote aging in C. elegans
New research from the Grishok Lab: spermatogenic Argonaute proteins are activated by Insulin/IGF-1 Signaling and promote aging in C. elegans
Congratulations to Stefan Isaac; one of the selected 2025 Toffler Scholars!
Congratulations to Stefan Isaac who was one of the selected 2025 Toffler Scholars!
The Toffler Scholar Program supports medical investigators engaged in early-stage, innovative medical research.
See announcement here:
Karen Toffler Charitable Trust Announces Toffler Scholars - Toffler Trust
New Research from the Layne Lab: mechanisms of adipose tissue fibrosis
A new study from the Layne laboratory identified a function for the transcription factor FOXS1 in regulating TGFb-dependent changes in adipogenic differentiation: JBC in press.
White adipose tissue (WAT) fibrosis is a major determinant of obesity-induced dysfunction and is characterized by excessive extracellular matrix deposition and myofibroblast activation. In this study, first author Alexander Tavares and co-authors identified FOXS1, a member of the forkhead box transcription factor superfamily, as a transcriptional target of TGF-β1 signaling in primary human adipocyte stem cells. FOXS1 also attenuated the induction of several adipogenic factors and sensitized cells to the anti-adipogenic effects of TGF-β1. Furthermore, loss of endogenous FOXS1 improved adipogenic permissiveness and activated proadipogenic gene programs in progenitors, even after TGF-β1 stimulation. These results indicate that FOXS1 is a positive regulator of profibrotic TGF-β1-dependent cellular responses, orchestrating the regulation of molecular phenotypes that promote myofibroblast activation and block adipogenesis. Co-authors in this study from the Layne lab include Scott Connelly, Daryn Maksat, Jane Zheng and Nabil Rabhi from the Farmer lab.
New news out of the Saeed Lab: Researchers Discover Protein Necessary for SARS-CoV-2 to Evade the Body’s Defenses
Congratulations to Barbara Schreiber being named educator of the year
Congratulations to Dr. Barbara Schreiber who has been named the 2025 Educator of the Year: PhD. 