Date: 16 November 2023 (Thursday)

Time: 5:00 pm – 6:00 pm

Venue: Seminar Room 609, 6/F, William M.W. Mong Block, 21 Sassoon Road

5:00 p.m.

Presenter: Ki Ki CHAM (MPhil candidate)
Primary Supervisor: Prof. Dong-Yan JIN
Presentation Title: Understanding the role of tail charge in MAVS localization and Type I Interferon signaling
Abstract: Mitochondrial Antiviral Signaling (MAVS) protein plays a vital role in innate immune responses by inducing type I interferon (IFN) and IFN-stimulated genes (ISGs). It has been reported that MAVS is present on both peroxisomes and mitochondria, and suggested that peroxisomal and mitochondrial MAVS act sequentially to establish an antiviral cellular state. However, the coordinated roles of mitochondrial MAVS and peroxisomal MAVS in type I IFN induction remain unclear. Additionally, it has been proposed that the subcellular localization of MAVS is determined by a combination of tail charge and transmembrane domain (TMD) hydrophobicity. This raises the question of whether changing the tail charge of MAVS alters its subcellular localization. To address these questions, we generate location-specific MAVS variants to investigate the antiviral activity of mitochondrial and peroxisomal MAVS, exploring their potential cooperation in type I IFN signaling.

5:30 p.m.

Presenter: Panpan WANG (PhD candidate)
Primary Supervisor: Dr. Lydia CHEUNG
Presentation Title: The functional role of nuclear p85β in transcriptional regulation
Abstract: The class IA PI3K consists of p110 catalytic and p85 regulatory subunits to initiate pathway activation, with p85α and p85β being the two major regulatory subunits.  Interestingly, in addition to its functional presence in the cytoplasm, p85β localizes to the nucleus. This study aims to understand the role of nuclear p85β. Excluding p85β from the nucleus using a nuclear export signal abolished the oncogenic effects of wild-type p85β. Multi-omics analysis identified BCL2-Associated Transcription Factor 1 (BCLAF1) as a downstream mediator of nuclear p85β. ChIP-seq analysis revealed co-occupancy of p85β and BCLAF1 at genomic loci including that of BCLAF1. This co-recruitment of BCLAF1 and p85β to BCLAF1 thereby activated BCLAF1 transcription, indicating a positive autoregulatory loop. These findings offer new insights into the mechanistic action of nuclear p85β, its interaction with the oncogenic transcription factor BCLAF1, and its impact on gene transcription in cancer.

ALL ARE WELCOME

Should you have any enquiries, please feel free to contact Jerry Siu at 3917 6912.