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Tony Cesare

@thecesarelab.bsky.social

Head of the Genome Integrity Unit, Children's Medical Research Institute. Professor, University of Sydney.

599 Followers  |  402 Following  |  85 Posts  |  Joined: 17.11.2024  |  1.9146

Latest posts by thecesarelab.bsky.social on Bluesky

Happy that @drmelaniew.bsky.social and I could play a small role in this lovely work led by @ssegurabayona.bsky.social. Please do give the preprint a look.

11.09.2025 08:35 β€” πŸ‘ 0    πŸ” 0    πŸ’¬ 0    πŸ“Œ 0
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πŸ“’Deadline extended!
Our 2nd Spatial Genome Organisation Conference deadline has been extended to 25 Sep, dont miss out on joining our fantastic line up of speakers, alongside Karim, Matthias and Irene in what is set to be a fantastic meeting this October! #SGO25
Final slots ➑️https://bit.ly/3JJzYR4

02.09.2025 14:34 β€” πŸ‘ 0    πŸ” 3    πŸ’¬ 1    πŸ“Œ 1

Lovely work Pragathi!

06.08.2025 00:56 β€” πŸ‘ 0    πŸ” 0    πŸ’¬ 0    πŸ“Œ 0

A shout out to lab member @szmyd-radoslaw.bsky.social for his recent recognition by @sydney.edu.au. Well earned Radek!

06.08.2025 00:55 β€” πŸ‘ 6    πŸ” 0    πŸ’¬ 0    πŸ“Œ 0
A person seated in a laboratory setting with shelves, containers, and scientific equipment in the background.

A person seated in a laboratory setting with shelves, containers, and scientific equipment in the background.

We’re proud of our researcher Dr Radek Szmyd who has received a 2025 University of Sydney Faculty of Medicine and Health Mid-Career Research Outstanding Publication Award - for Radek’s extraordinary work to understand why cancer cells die in different ways following radiotherapy.

17.07.2025 06:59 β€” πŸ‘ 1    πŸ” 1    πŸ’¬ 0    πŸ“Œ 1
DNA-repair-driven cell death compels us to rethink cancer therapies - Nature Reviews Molecular Cell Biology Emerging evidence suggests that, following genotoxic therapy, it is the repair of DNA double-strand breaks, rather than the damage itself, that frequently drives cancer cell death.

New from us in @natrevmcb.nature.com -- @szmyd-radoslaw.bsky.social & @radoncdocgee.bsky.social explore how DNA repair actively shapes cancer cell fate following DNA damage, reframing repair as both a protective process & a driver of treatment response and cell death. www.nature.com/articles/s41...

04.08.2025 05:48 β€” πŸ‘ 25    πŸ” 9    πŸ’¬ 1    πŸ“Œ 1

DNA replication and Cryo-EM star Jacob Lewis is visiting @cmri.bsky.social today to present seminar. If you happen to be in Westmead, talk is 12:30 pm local time. See you there.

20.06.2025 01:54 β€” πŸ‘ 0    πŸ” 0    πŸ’¬ 0    πŸ“Œ 0
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Hunter Meeting 2025

Excited to speak at the Hunter Meeting next week, alongside @cmri.bsky.social colleagues Pragathi Masamsetti (postdoc with Patrick Tam, proud Cesare lab alum) and Pengyi Yang (Head, Computational Systems Biology Unit). Looking forward to great science and good company.

www.huntermeeting.org.au

27.05.2025 01:56 β€” πŸ‘ 3    πŸ” 1    πŸ’¬ 0    πŸ“Œ 0
Home | acpc

If you happen to be the the Oz Single Cell Conference this week in Sydney, check out @scientistkate.bsky.social's talk on Friday.

Kate is a joint postdoc w/@piptaberlay.bsky.social and will present her work on 3D Genome architecture and replication stress.

www.ozsinglecell.com

19.05.2025 23:26 β€” πŸ‘ 3    πŸ” 1    πŸ’¬ 0    πŸ“Œ 0

ACCM 2025! The Cesare lab will be there in force. Come join us in Melbourne for 3 days of amazing science.

15.05.2025 12:36 β€” πŸ‘ 0    πŸ” 0    πŸ’¬ 0    πŸ“Œ 0
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I'm super excited to announce that registrations are now open for the 19th Australian Cell Cycle, DNA Repair and Telomere Workshop. Awesome international speaker line-up, with plenty of locals being invited! Book now to secure your earlybird rate. www.australiancellcycle.org

15.05.2025 05:48 β€” πŸ‘ 17    πŸ” 9    πŸ’¬ 1    πŸ“Œ 3

Fantastic opportunity in Melbourne.

14.05.2025 11:55 β€” πŸ‘ 3    πŸ” 1    πŸ’¬ 0    πŸ“Œ 0

Hosting Lee Wong from @monashuniversity.bsky.social tomorrow to present her seminar: "Onco-histone mutations in paediatric high-grade glioma: molecular mechanisms and implications for therapy." If you are around @cmri.bsky.social tomorrow at 12:30, come by for a great talk.

08.05.2025 01:32 β€” πŸ‘ 3    πŸ” 0    πŸ’¬ 0    πŸ“Œ 0

@genomestability.bsky.social (Andrew Deans) will be @cmri.bsky.social tomorrow to present seminar at 12:30; "The Multifaceted Role of FANCM enzyme in DNA Repair and Cancer Therapy". If you are in the area, please do come by for a great talk.

10.04.2025 05:23 β€” πŸ‘ 6    πŸ” 1    πŸ’¬ 0    πŸ“Œ 0

Sorry Sam and @jenniferlovesecoli.bsky.social, I am also unaware of papers/studies exploring nuclear F-actin in c. elegans. Happy to be updated if anyone knows otherwise.

21.03.2025 00:29 β€” πŸ‘ 3    πŸ” 0    πŸ’¬ 1    πŸ“Œ 0

*basketball... πŸ€¦β€β™‚οΈ

21.03.2025 00:15 β€” πŸ‘ 0    πŸ” 0    πŸ’¬ 0    πŸ“Œ 0
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My and @telomerase-cmri.bsky.social’s annual attempt to bring a little bit of college baseketball culture down under.

Go Tar Heels!

20.03.2025 22:17 β€” πŸ‘ 10    πŸ” 1    πŸ’¬ 1    πŸ“Œ 0
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Nuclear and genome dynamics underlying DNA double-strand break repair Nature Reviews Molecular Cell Biology - Changes in nuclear and genome organization promote the repair of DNA double-strand breaks and genome stability. Processes that are involved include the...

πŸš€ New Paper Alert! Our latest @natrevmcb.bsky.social explores how nuclear and genome organization drive DNA double-strand break repair! 🧬

πŸ“– Free access: rdcu.be/edViW

Please πŸ”„ ❀️

18.03.2025 13:49 β€” πŸ‘ 58    πŸ” 24    πŸ’¬ 1    πŸ“Œ 0
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A CPC-shelterin-BTR axis regulates mitotic telomere deprotection Nature Communications - Here the authors reveal how telomeres signal mitotic stress. A key protein network alters their structure exposing telomere ends to signal mitotic stress, ultimately...

🧡 1/10 Excited to share our latest study in @naturecomms.bsky.social
"A CPC-shelterin-BTR axis regulates mitotic telomere deprotection" t.co/VypPsLBJCR

17.03.2025 12:49 β€” πŸ‘ 10    πŸ” 4    πŸ’¬ 1    πŸ“Œ 0

26/Finally, the data are consistent with t-loops suppressing ATM activation by the chromosome end.

T-loops opening in a regulated and shelterin-dependent manner to signal cellular stress suggests a broader role for these chromosome end structures than previously appreciated.

17.03.2025 10:32 β€” πŸ‘ 2    πŸ” 0    πŸ’¬ 1    πŸ“Œ 0

25/We predict this represents a non-canonical telomere-dependent tumour suppressive activity outside the canonical ageing-dependent proliferative barriers imposed by telomere erosion.

Additionally, we found the protective functions of the TRF2 basic domain are mitosis specific.

17.03.2025 10:32 β€” πŸ‘ 1    πŸ” 0    πŸ’¬ 1    πŸ“Œ 0

24/What does this mean?

We now understand the pathway of MAD-telomere deprotection that contributes to 1) cell death during mitotic arrest, and 2) p53-dependent cell cycle arrest when cells escape an elongated mitosis.

17.03.2025 10:32 β€” πŸ‘ 1    πŸ” 1    πŸ’¬ 1    πŸ“Œ 0
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23/Live imaging from both labs revealed that TRF2 mutants that suppress MAD-telomere deprotection also reduce the prevalence of mitotic arrest driven lethality. While TRF2 mutants that promote MAD-telomere deprotection enhanced mitotic death or expedited time of mitotic arrest to lethality.

17.03.2025 10:32 β€” πŸ‘ 0    πŸ” 0    πŸ’¬ 1    πŸ“Œ 0
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22/Of note, telomeres do not rapidly truncate in MAD-telomere deprotection like they do when the TRF2 basic domain is deleted. Thus, while the TRF2 basic domain is modified to enable BTR-dependent t-loop opening, it does not allow t-loop junction cleavage, consistent with a highly regulated pathway.

17.03.2025 10:32 β€” πŸ‘ 0    πŸ” 0    πŸ’¬ 1    πŸ“Œ 0
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21/Diana’s molecular biology was consistent with the BTR complex being requisite for MAD-telomere deprotection following TRF2 modification.

This suggested that t-loops junctions are in a double Holliday Junction configuration during mitotic arrest before resolution by BTR.

17.03.2025 10:32 β€” πŸ‘ 0    πŸ” 0    πŸ’¬ 1    πŸ“Œ 0
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20/How does BLM fit into the story?

BLM does many things, including double Holliday Junction dissolution (dHJ) via the BTR complex. T-loops are typically drawn with strand-invasion promoting a displacement loop. However, this is conjecture, and the t-loop junction identify is unknown.

17.03.2025 10:32 β€” πŸ‘ 0    πŸ” 0    πŸ’¬ 1    πŸ“Œ 0
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19/Ronnie's Airyscan imaging of telomere macromolecular structure following in situ trioxsalen cross-linking and chromatin spreading suggested TRF2 basic domain phosphorylation promoted the transition from looped to linear telomeres during mitotic arrest, coinciding with telomere DDR induction.

17.03.2025 10:32 β€” πŸ‘ 0    πŸ” 1    πŸ’¬ 1    πŸ“Œ 0
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18/Critically, both labs showed that all TRF2 S62 and/or S65 phospo-null or phospho-mimetic mutants retained interphase telomere protection, indicating these residues function specifically in mitotic telomere protection. Diana & Makoto also showed that TRF1 and TRF2 mutants localized to telomeres.

17.03.2025 10:32 β€” πŸ‘ 1    πŸ” 0    πŸ’¬ 1    πŸ“Œ 0
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17/Sam created a phosphospecific antibody against pTRF2-S65 and his biochemistry confirmed this residue was phosphorylated specifically during mitotic arrest in an AURKB-dependent fashion.

17.03.2025 10:32 β€” πŸ‘ 0    πŸ” 0    πŸ’¬ 1    πŸ“Œ 0

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