Jason Wong

Now out at #jbiolchem www.sciencedirect.com/science/arti...

Our full-day mini AI hackathon on genomic language models starts soon: 8.30am-8.30pm! With a whole team, we aim to test how gLMs work for two tasks:
1. SNP2GEX: personal variants to gene expression (unseen individuals & genes);
2. Seq2CellxTF: short regulatory to TF binding (unseen cell & TFs).

LocusMasterTE: integrating long-read RNA sequencing improves locus-specific quantification of transposable element expression - Genome Biology Transposable elements (TEs) can influence human diseases by disrupting genome integrity, yet their quantification has been challenging due to the repetitive nature of these sequences across the genome...

Great to finally see LocusMasterTE in print by PhD student, Sojung Lee. We developed a bioinformatics method to leverage long read sequencing data to improve expression quantification of transposable elements genomebiology.biomedcentral.com/articles/10.... #GenomeBiology

GitHub - jasonwong-lab/LocusMasterTE: Integrating long read sequencing enhances short read-based locus-specific transposable element quantification Integrating long read sequencing enhances short read-based locus-specific transposable element quantification - GitHub - jasonwong-lab/LocusMasterTE: Integrating long read sequencing enhances sho...

Open source @github.com github.com/jasonwong-la.... And thank you @yuanhuahuang.bsky.social for the amazing collaboration!

A case where the oodles of public lung cell line data generated as a result of COVID can be put to good use in cancer! Well done to Sojung Lee (PhD student), for the massive effort in data mining. (9/n)

Given that ERVK-7 expression is a potential biomarker for ICB response in LUAD, ERVK-7.long may be a more specific and easier to quantify. Controlling the epigenetic regulation of ERVK-7.long may also alter the immune microenvironment of LUAD. (8/n)

In addition to cell type specificity, the promoter of ERVK-7.long is driven by NF-κB, likely via TNF-α, while ERVK-7.short is already known to be regulated by IRFs. (7/n)

The promoter of ERVK-7.long was found to be lineage-specific, with H3K4me3 deposition in LUAD cells. ScRNA-seq confirmed that ERVK-7.long expression is restricted largely to LUAD cells, fibroblasts, and AT-2 cells, which may be the cell type of origin of LUAD cells. (6/n)

ERVK-7.long is highly expressed in LUAD, contributing significantly to the overall expression of ERVK-7. This suggests that the epigenetic regulation of ERVK-7.long may be key to ERVK-7 overexpression in patients. (5/n)

HERVs and retroviruses are transcribed from the 5'LTR. Yet PacBio Iso-seq revealed alternative transcripts for ERVK-7 arising from upstream promoters, with the canonical TSS of the 5'LTR heavily methylated in A549 (ONT WGS) along with TFBS mutations. (4/n)

A key motivation for us is to understand the epigenetic regulation of ERVK-7 as it is frequently over-expressed but only amplified in ~10% of LUAD patients. (3/n)

HERVs are generally silent or dysfunctional in the human genome. Yet recent studies have shown that the expression of certain copies, such as ERVK-7 (HERV-K102), is associated with autoantibodies and immunotherapy response in lung cancer patients t.co/21yyHijgMd. (2/n)

First post on Bluesky 🦋. Happy to share some new work on the epigenetic regulation of a human endogenous retrovirus (HERV) in cancer. @biorxivpreprint.bsky.social bsky.app/profile/bior... 🧵 (1/n)