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Mathew Jones

@jonesmjk.bsky.social

Investigating kinase-dependent regulation of DNA replication and repair

120 Followers  |  410 Following  |  5 Posts  |  Joined: 22.08.2025  |  1.608

Latest posts by jonesmjk.bsky.social on Bluesky

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AI-powered genomics platform brings hope for better cancer treatments Researchers from the University of Queensland and University of Cambridge have developed a platform for human cells powered by artificial intelligence that could aid the development of therapeutics an...

Pleased to see our latest research highlighted news.uq.edu.au/2025-10-ai-p...

09.10.2025 12:44 β€” πŸ‘ 0    πŸ” 0    πŸ’¬ 0    πŸ“Œ 0
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For decades, human genome editing has been limited to small, localized modifications.

Today, in a new paper published in @science.org , researchers from Arc's Hsu lab show that bridge recombinase technology is capable of large-scale genomic rearrangements in human cells.

25.09.2025 18:27 β€” πŸ‘ 23    πŸ” 14    πŸ’¬ 2    πŸ“Œ 0
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Systematic discovery of CRISPR-boosted CAR T cell immunotherapies - Nature CELLFIE, a CRISPR platform for optimizing cell-based immunotherapies, identifies gene knockouts that enhance CAR T cell efficacy using in vitro and in vivo screens.

CAR T cells showcase the enormous potential of cell therapies, but often fail due to lack of evolutionary optimization. Today in @nature.com , we use #CELLFIE to engineer cell therapies at scale and share the largest resource of CRISPR screens in CAR T cells. www.nature.com/articles/s41...

24.09.2025 15:44 β€” πŸ‘ 4    πŸ” 3    πŸ’¬ 1    πŸ“Œ 1

Fantastic meeting with an excellent line up of speakers. Come join us for the Australian Cell Cycle meeting in Melbourne.

25.09.2025 02:03 β€” πŸ‘ 5    πŸ” 3    πŸ’¬ 0    πŸ“Œ 1
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DNA methylation influences human centromere positioning and function - Nature Genetics Genome-wide and targeted perturbation of DNA methylation at centromeres affects CENP-A positioning and centromere structure, resulting in aneuploidy and reduced cell viability.

#1 Centromeres are epigenetic loci defined by CENP-A, positioned in unmethylated DNA flanked by highly methylated regions. Our work, published in @natgenet.nature.com in collaboration with @naltemose.bsky.social investigates the role of DNAme at human centromeres www.nature.com/articles/s41...

04.09.2025 13:10 β€” πŸ‘ 82    πŸ” 35    πŸ’¬ 9    πŸ“Œ 1
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An electrostatic repulsion model of centromere organisation During cell division, chromosomes reorganise into compact bodies in which centromeres localise precisely at the chromatin surface to enable kinetochore-microtubule interactions essential for genome se...

1/ New preprint alert!
In collaboration between the Rosen, Redding, Collepardo-Guevara & Gerlich labs, we uncover a surprising principle of chromosome organisation: electrostatic repulsion positions centromeres at the chromosome surface during mitosis.
πŸ”— doi.org/10.1101/2025...

03.09.2025 08:11 β€” πŸ‘ 62    πŸ” 26    πŸ’¬ 2    πŸ“Œ 2
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Australian Invited Speakers 2025 We are in the process of inviting a number of outstanding Australian leaders in the fields of DNA repair, Cell Cycle and Telomere biology. Current invited speakers include: Lisa Alcock, Curtain Uni…

🦘🧬Australian invited speaker list finalised for the
2025 Cell Cycle, DNA repair and Telomere Meeting!
Friday 5 Sep is your last chance to register at the EARLY BIRD rate & submit an abstract 🀩
australiancellcycle.org/australian-i...

03.09.2025 22:42 β€” πŸ‘ 11    πŸ” 4    πŸ’¬ 1    πŸ“Œ 1

Thanks Gideon! It was a long time coming and more improvements to follow.

01.09.2025 13:59 β€” πŸ‘ 0    πŸ” 0    πŸ’¬ 0    πŸ“Œ 0
The balance between B55Ξ± and Greatwall expression levels predicts sensitivity to Greatwall inhibition in cancer cells - Nature Communications The authors develop and characterise a selective Greatwall inhibitor, C-604, and show that its cytotoxicity stems from PP2A-B55Ξ± hyperactivation. They identify B55Ξ± and Greatwall levels as biomarkers…

Excited to share our new @NatureComms paper! We developed C-604, a selective inhibitor of Greatwall kinase, and discovered that cancer cells' sensitivity to it depends on a simple ratio: B55Ξ±/Greatwall expression levels.
www.nature.com/articles/s41...

28.08.2025 11:07 β€” πŸ‘ 15    πŸ” 7    πŸ’¬ 3    πŸ“Œ 0
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The paper builds on our preprint with DNAscent v4 on R10.4.1 chemistry with improved BrdU and EdU detection and fork calling.

01.09.2025 10:04 β€” πŸ‘ 0    πŸ” 0    πŸ’¬ 0    πŸ“Œ 0
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A high-resolution, nanopore-based artificial intelligence assay for DNA replication stress in human cancer cells Nature Communications - Determining how replication forks move across the human genome is critical for the effective use of agents that target replication stress. Here, the authors present...

Checkout our latest research in @natcomms.nature.com
rdcu.be/eBqBI A high-resolution, nanopore-based artificial intelligence assay for DNA replication stress in human cancer cells. A collaboration with Mike Boemo’s team

01.09.2025 10:04 β€” πŸ‘ 30    πŸ” 15    πŸ’¬ 2    πŸ“Œ 0
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JOB ALERT 🚨 We are hiring TWO principal investigators in cell, molecular, systems, or chemical biology in Toronto, Canada at @sinaihealth.bsky.social. We provide a generous startup, fully funded salary and academic appointment at U of Toronto.

www.nature.com/naturecareer...

Please repost!

28.08.2025 06:34 β€” πŸ‘ 130    πŸ” 169    πŸ’¬ 0    πŸ“Œ 7
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Centromere protection requires strict mitotic inactivation of the Bloom syndrome helicase complex Nature Communications - Centromeres play an essential function in faithful chromosome segregation. Here, the authors demonstrate the mechanism by which human cells dynamically modulate the activity...

#NEW_PAPER

In this study, the Chan Lab uncover the molecular mechanisms by which human cells safeguard centromeric chromatin during mitosis, via tight dynamic control of the Bloom Syndrome complex (BTRR).

rdcu.be/eCGxF

27.08.2025 11:16 β€” πŸ‘ 11    πŸ” 5    πŸ’¬ 0    πŸ“Œ 2
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The mitotic STAG3–cohesin complex shapes male germline nucleome - Nature Structural & Molecular Biology Nagano et al. identify the third mitotic cohesin complex, STAG3–cohesin, which, with its unique biophysical properties, weakens insulation and rewires regulatory interactions of spermatogonial stem ce...

This insightful manuscript implicating STAG3 in mitotic, rather than the known meiotic, control of chromatin architecture came out a couple of days ago. Glad to see it in our pages @natsmb.nature.com and I am looking forward to see what the community will think www.nature.com/articles/s41...

27.08.2025 10:49 β€” πŸ‘ 6    πŸ” 4    πŸ’¬ 0    πŸ“Œ 0
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A redox switch in p21-CDK feedback during G2 phase controls the proliferation-cell cycle exit decision ROS oxidize cell cycle proteins and regulate cell proliferation. Vorhauser et al. show that oxidation of the cyclin-dependent kinase (CDK) inhibitor p21 at cysteine 41 (C41) during the G2 phase controls its stability. Loss of C41 oxidation increases p21 stability, impairs proliferation, and promotes senescence after irradiation.

Online Now: A redox switch in p21-CDK feedback during G2 phase controls the proliferation-cell cycle exit decision Online now:

26.08.2025 19:17 β€” πŸ‘ 9    πŸ” 4    πŸ’¬ 0    πŸ“Œ 1
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Targeting G1–S-checkpoint-compromised cancers with cyclin A/B RxL inhibitors - Nature Dual cyclin A/B RxL inhibitors selectively kill small cell lung cancer cells and other cancer cells with high E2F activity.

Nature research paper: Targeting G1–S-checkpoint-compromised cancers with cyclin A/B RxL inhibitors

go.nature.com/45JauuG

22.08.2025 18:29 β€” πŸ‘ 14    πŸ” 3    πŸ’¬ 0    πŸ“Œ 0
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Snoozing APC/C for a sweet cell cycle entry Nature Reviews Molecular Cell Biology, Published online: 21 August 2025; doi:10.1038/s41580-025-00891-8Paul et al. demonstrate that entry into the cell cycle from quiescence involves a transient, partial inactivation of the APC/C ubiquitin ligase, which halts the degradation of glycolysis enzymes and ensures sufficient ATP production for cell division.

ICYMI: New Online! Snoozing APC/C for a sweet cell cycle entry

24.08.2025 11:38 β€” πŸ‘ 3    πŸ” 1    πŸ’¬ 0    πŸ“Œ 0

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