Department of Pharmacology Works in Progress:
Speaker: Caleb Embree, PhD Postdoctoral fellow in the lab of Katherine Borden, PhD
Title: "Mismatched SOCCS: Nuclear eIF4E and NCBP2 govern distinct fates for 1000s of mRNAs uncovering an unexpected regulatory point in gene expression"
Abstact: Protein coding transcripts possess 5’ m7G “cap” which are recognized by cap-binding proteins that shepherd mRNAs through the major mRNA processing steps, RNA export and translation. Both the cap binding complex (CBC) made of the NCBP2/NCBP1 heterodimer and eIF4E are present in the nucleus and play a role in mRNA processing. To determine if these two cap-chaperones are functionally redundant we overexpressed NCBP2 and eIF4E in U2OS cells and examined how they affected pre-mRNA splicing. We found that the two proteins regulate distinct alternative splicing programs, suggesting a novel regulatory mechanism we have named specification of cap-chaperones (SOCCS), whereby cap-chaperones regulate the processing of specific subsets of mRNA.
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Speaker: Vernon Kennedy MD-PhD Candidate in the lab of Murali Prakriya, PhD
Title: "Orai1-mediated SOCE in the Choroid Plexus and its Role in Neuroinflammation"
Abstract: Calcium (Ca2+) is a key second messenger regulating cellular processes, including vesicular exocytosis, gene expression, and cell homeostasis. Store-operated Ca2+ entry (SOCE), mediated by Orai1 channels, is a major Ca2+ entry pathway in most cells. In the brain, Orai1 is highly expressed in the choroid plexus (CP), which produces cerebrospinal fluid, maintains the blood-CSF barrier, and plays a central role in CNS immune surveillance. Using pharmacological and genetic approaches with calcium imaging, I demonstrate that Orai1 is essential for SOCE and serotonin-induced Ca2+ signals in the CP epithelium, and that it regulates proinflammatory gene expression and barrier remodeling, identifying Orai1 as a key mediator linking serotonin signaling to CP immune function and neuroinflammation.
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