Houseley Lab
@houseleylab.bsky.social
140 followers 170 following 11 posts
We study molecular mechanisms of ageing and adaptation. @BabrahamInst, Cambridge, UK. Main funding @BBSRC Views are our own.
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houseleylab.bsky.social
6-way multiplexing at the first step allows 10-20 libraries to be made in parallel

Great work Neesha and thanks to our collaborators and our funders
houseleylab.bsky.social
TrAEL-seq read density reflects the speed or replication forks, allowing quantification of interactions with genomic elements such as transcription
houseleylab.bsky.social
Our new Preprint describes an improved TrAEL-seq protocol:

• Provides far better data from mammalian cells

• Includes multiplexing for higher throughput

TrAEL-seq reveals replication patterns and fork progression in unsynchronised, unlabelled and unsorted cells

www.biorxiv.org/content/10.1...
houseleylab.bsky.social
If you're at the AGE meeting don't miss the BSRA Korenchevsky Award talk from Hanane Hadj-Moussa!

Hanane's work shows that we can acheive excellent healthy ageing through metabolic rewiring, even on an unrestricted diet

Profile:
whova.com/embedded/spe...

Preprint:
www.biorxiv.org/content/10.1...
houseleylab.bsky.social
Great work lead by Hanane Hadj-Moussa and Megan Ulusan

Babraham Institute @babrahaminst.bsky.social

#BBSRC @ukri.org
houseleylab.bsky.social
AMPK orchestrates responses to low nutrient availability from yeast to humans…

…including regulation of fatty acid synthesis through phosphorylation of the same enzyme

This highly conserved regulatory system presents a promising and unexplored target for healthy ageing research across Eukaryotes
houseleylab.bsky.social
Controlling Acetyl coenzyme A availability underlies all these effects

Acetyl coenzyme A is the building block for fatty acids but excess acetyl coenzyme A availability is detrimental

A2A cells make the fatty acid they need but get rid of excess acetyl coenzyme A into mitochondria
houseleylab.bsky.social
but AMPK activation turns off fatty acid production, which is a problem

Our A2A mutant combines AMPK activation with a mutation that allows continued fatty acid synthesis

The majority of A2A cells maintain fitness very late in life even though they don't live any longer
houseleylab.bsky.social
AMPK activity is widely considered to be beneficial for ageing health

We show that AMPK activation in budding yeast allows some cells to age without senescence on a normal diet...
houseleylab.bsky.social
Is healthy ageing possible on a normal diet?

Our latest Preprint describes metabolic re-engineering of yeast to avoid senescence

The A2A mutant we created is super-fit late in life even on a rich high glucose diet

www.biorxiv.org/content/10.1...
houseleylab.bsky.social
Congratulations to our PhD student Amy Wolstenholme for winning the Poster Prize at the EMBL Drug Resistance meeting #EESDrugResistance this week

Amy's poster showed that circular DNAs providing copper resistance can be stably transmitted for hundreds of generations in yeast