Stirling Churchman

Single-minus gluon tree amplitudes are nonzero Single-minus tree-level $n$-gluon scattering amplitudes are reconsidered. Often presumed to vanish, they are shown here to be nonvanishing for certain "half-collinear" configurations existing in Klein...

arxiv.org/abs/2602.12176

GPT-5.2 derives a new result in theoretical physics A new preprint shows GPT-5.2 proposing a new formula for a gluon amplitude, later formally proved and verified by OpenAI and academic collaborators.

I watched Andy go from, "I was invited to OpenAI for a week, what should I get Chat to help me with?" to an exciting new result and preprint in under a month!

I'm excited for Andy and the new speed at which physics can be done!
openai.com/index/new-re...

Hope to see you at one of my favorite meetings! Deadline extended to tomorrow!!

One day left till submit an Abstract!

Join @stirlingchurchman.bsky.social,
@moffittlab.bsky.social, @saramostafavi.bsky.social, me and all speakers for the 2026 CSHL meeting Systems Biology: Global Regulation of Gene Expression, March 11-14. Abstract deadline January 9! More infos and registration at meetings.cshl.edu/meetings.asp...

Mapping single-cell diploid chromatin fiber architectures using DAF-seq - Nature Biotechnology Single-molecule chromatin fiber sequencing exposes single-cell-level heterogeneity in the chromatin architecture of individual regulatory elements.

Mapping single-cell diploid chromatin fiber architectures using DAF-seq - @uwgenome.bsky.social @uwdeptmedicine.bsky.social go.nature.com/4rFTAHy

Translational activators align mRNAs at the small mitoribosomal subunit for translation initiation Nature Structural & Molecular Biology - Mitochondrial translational activators (TAs) facilitate transcript-specific translation. Using selective ribosome profiling and cryo-electron microscopy,...

Our study on the molecular function of translational activators for mitochondrial protein synthesis is published:
rdcu.be/eSWxT
A great collaboration with @stirlingchurchman.bsky.social and @sshaolab.bsky.social with structural work from our @pelleeas.bsky.social
Funded by @kawresearch.bsky.social

While these mechanisms are beautiful, they likely don't operate in human mitochondria, which have lost 5' UTRs entirely. How the mito-nuclear partnership is resolved in human cells remains a fascinating question. Stay tuned...

A molecular switch at the yeast mitoribosomal tunnel exit controls cytochrome b synthesis Abstract. Mitochondrial gene expression needs to be balanced with cytosolic translation to produce oxidative phosphorylation complexes. In yeast, translati

Mrx4 binds either the translational activators or the assembly factor Cbp3-Cbp6, but not both. This toggles COB translation on or off depending on whether newly synthesized cytochrome b can be assembled. academic.oup.com/nar/article/...?

In a companion paper, we asked a another question: how is translation coupled to the availability of nuclear-encoded subunits? Carlström, Bridgers et al. identified Mrx4 as a molecular switch at the polypeptide tunnel exit that controls cytochrome b translation.

Translational activators align mRNAs at the small mitoribosomal subunit for translation initiation Nature Structural & Molecular Biology - Mitochondrial translational activators (TAs) facilitate transcript-specific translation. Using selective ribosome profiling and cryo-electron microscopy,...

We show that translational activators bind the 5' UTR of their client mRNA and dock at the mRNA channel exit on the small subunit, positioning the start codon in the P-site. Cryo-EM structures revealed how TAs wrap around the 5' UTR and contact the ribosome to align the mRNA. rdcu.be/eSWxT

In a paper published today, we asked: mitochondrial mRNAs lack Shine-Dalgarno sequences, so how do mitoribosomes find the start codon? Bridgers, Carlström, Sherpa et al. @pelleeas.bsky.social @sshaolab.bsky.social

The unique attributes of the mitochondrial genome and the mitochondrial ribosome renders OXPHOS synthesis and co-translational assembly difficult to study, so we established selective mitoribosome profiling to study mitochondrial translation regulation in its native context.

Oxidative phosphorylation complexes contain subunits encoded by both the nuclear and mitochondrial genomes. How do cells coordinate the synthesis and assembly of these complexes at the inner membrane? We teamed up with Martin Ott (@mitolab.bsky.social) to address this in two recent papers.

An exciting study driven by the close collaboration of first authors @erinduffyphd.bsky.social and @inespatop.bsky.social. And thanks to our other colleagues for making this such a comprehensive study. (11/11)

This work reveals RNA stability as a "hidden layer" of gene regulation that: 1) Operates independently of transcription 2) Works locally in neuronal processes 3) Is disrupted in neurodevelopmental disorders 4) Expands our view of activity-dependent plasticity (10/11)

Importantly, HuD-bound mRNAs are enriched for autism spectrum disorder (ASD) risk genes, and ASD variants can alter RNA stability regulation, implicating this pathway in neurodevelopmental disorders. (9/11)

How does activity change HuD function? Not by changing HuD levels, but by reorganizing its protein partners. Microscopy and IP-MS support a model where activity recruits HuD into RNA granules, stabilizing HuD-bound mRNAs by protecting them from degradation. (8/11)

We found that activity-dependent gene expression is modulated in both soma and distal processes (dendrites and axons), suggesting neurons may coordinate RNA stability, transport, and translation to adjust protein levels locally. (7/11)

To gain some mechanistic insight, we used MPRAs, machine learning, RIP-seq and metabolic labeling and identified the RNA binding protein HuD as a key regulator of activity-dependent RNA stability. (6/11)

And we did some in vivo validation: We also see effects on RNA stability in vivo in response to novel environment exploration, meaning this isn’t just a phenomenon in primary neurons, it also occurs in a physiologically relevant learning paradigm in the intact brain. (5/11)

RNA stability changes weren’t just a side effect. For ~10% of activity-dependent transcripts, stability mattered more than transcription for determining RNA levels, challenging the transcription-centric view of gene regulation in this process. (4/11)

Of ~5,000 activity-regulated transcripts, two thirds showed changes in transcription, which was expected. Unexpectedly, ~1,000 genes were regulated by RNA stability.(3/11)

When neurons fire, they need to rapidly change which genes are expressed to support processes like long-term memory. Transcriptional responses are well studied, but what about other steps in the RNA life cycle? (2/11)

HuD controls widespread RNA stability to drive neuronal activity-dependent responses Neuronal activity shapes brain development and refines synaptic connectivity in part through dynamic changes in gene expression. While activity-regulated transcriptional programs have been extensively...

Our new pre-print from the Greenberg and Churchman labs shows that activity-dependent modulation of RNA stability is a major, and underappreciated, mechanism of gene regulation in neurons. Tutorial below! www.biorxiv.org/content/10.1... (1/11)

I was inspired and made one last night! So good.

I'm late to this! That's the real deal! Go make a 1919 ASAP. :)

First time posting here — and first-ever Single Molecule Conference 🧬

Held right at @embl.org Heidelberg, where I work!

4 days full of great science and great people. Fantastic meeting! 🔬

Curious to see where the single molecule field is going next! 👀

#EMBLSingleMolecule @events.embl.org

Honored to receive 1st Place Poster Award 🏆 at the EMBL meeting "Gene Regulation: One Molecule at a Time"!
Thank you to all who visited and engaged in exciting discussions.
Grateful to the organizers for an excellent event! #EMBLSingleMolecule