🧑‍🔬Paper alert: In our latest paper published in @JHepatology, we explored the regulatory network in #hepatocyte ploidy during #ageing. 👇(1/10)

Well done and congratulations to @adelynechan, Narita lab and all authors involved! https://t.co/gwK5aoooci

🔬Fantastic three days at #CIMT2024 in Mainz, Germany. #immunotherapy is so wild 🤯🫠😂. bis nächstes Mal!

This work was co-led with @marenbuettner, best computational partner one could ask for! I would also like to extend my gratitude to @celia4science, @odom_lab, @fabian_theis for their guidance on the project, and spending countless hours in the writing zoom with me! (10/10)

Our work suggests that novel therapeutic interventions aimed at attenuating age-related changes in tissue function could be exploited by manipulation of #ploidy dynamics during chronic liver conditions. (9/10)

Using #BaseScope, we observed numerous tetraploid nuclei carrying wild-type alleles in aged #Hnf4a haploinsufficient hepatocytes, revealing non-random allele segregation post-genomic perturbation and demonstrating tetraploid hepatocytes' role in buffering genomic changes. (8/10)

In all mouse strains, we found improved lipid homeostasis and reduced transcriptomic variability in tetraploid hepatocyte nuclei from haploinsufficient mice, suggesting their involvement in genomic optimization during ageing. (7/10)

Crucially, although snRNA-seq2 analysis unveiled distinct gene expression profiles, the shared occurrence of early polyploidization in hepatocytes across all three haploinsufficient strains suggests a unified cellular state in mitigating ageing-related liver steatosis. (6/10)

Testing if early polyploidization extends beyond liver-specific master regulator haploinsufficiency, we studied a third haploinsufficient strain missing Ctcf. We found that Ctcf haploinsufficient mice also displayed improved lipid homeostasis and early polyploidization. (5/10)

To test this, we generated two haploinsufficient mice strains, each missing one allele of liver-specific master regulators, such as Hnf4a or Cebpa. We found that these mice showed improved lipid homeostasis and early polyploidization, despite the haploinsufficiency. (4/10)

Hepatocyte polyploidy, known to enhance cell survival upon severe injury, possibly also influences hepatocyte responses to non-deleterious genomic perturbation during lifespan. (3/10)

In wild-type mice, ageing causes hepatic fat accumulation and increased hepatocyte ploidy. Our analysis of hepatocyte nuclei via snRNA-seq2 reveals a heighted liver-specific regulatory networks in tetraploid nuclei during ageing. (2/10).

⭐️ I am thrilled to announce that the new and unique book “Sinusoidal cells in liver diseases” is finally out❗️ 25 chapters - 562 pages of updated translational & clinical science focused on the cells living in the sinusoidal milieu Get yours here! 🔗 https://t.co/QWuHegSbf7

Very happy to see the main paper from @A_L_Wilkinson's PhD now published in @iScience_CP. 🥳 @MIDASUoB @BirminghamLiver @ImmunologyUoB https://t.co/KcEksXQznP

Amazing #postdoc opportunity for scientists interested in developing their #omics and #hepatology skills in a fantastic lab.

Behind the scene 👨🏼‍🔬

🎬 and that’s a wrap! ⭐️ Check out our video protocol on isolating nuclei from bio banked tissues published in JoVE, starring our PhD student Mateusz from @MolAgeingLab 👇🏼 https://t.co/i78mhkyaFu

Stressed plants emit airborne sounds that can be detected from over a meter away. Lilach Hadany @YovelBatLab @TelAvivUni Learn more in @CellCellPress: https://t.co/Xxp19bcY0h

Beethoven’s cause of death revealed from locks of hair

Delighted to share our latest collab project led by ⁦@johwirth⁩ with ⁦@Meier_Lab⁩. 🤩 #spatial #transcriptomic #DBiTseq Check it out👇🏼 Spatial transcriptomics using multiplexed deterministic barcoding in tissue | Nature Communications