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Reposted by Jeff Mold

Natanael Spisak @natanaels.bsky.social · Sep 3

Very happy to share our work on signature SBS5. See Molly's thread for a short summary

Molly Przeworski @mollyprz.bsky.social · Sep 2

In these dark times, it comes as a rare pleasure to highlight @natanaels.bsky.social ‬ & @marcdemanuel.bsky.social's work on germline and somatic mutations in humans. 1/n
www.biorxiv.org/cgi/content/...

Collateral mutagenesis funnels multiple sources of DNA damage into a ubiquitous mutational signature

Mutations reflect the net effects of myriad types of damage, replication errors, and repair mechanisms, and thus are expected to differ across cell types with distinct exposures to mutagens, division ...

www.biorxiv.org

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Jeff Mold @jeffmold.bsky.social · 1d

It’s one thing to be wrong but a totally different thing to push crazy theories in the real scientific literature without doing even a modest amount of negative hypothesis testing. This is the real world outcome of the impact chasing game we have created in science…

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Jeff Mold @jeffmold.bsky.social · 1d

pmc.ncbi.nlm.nih.gov/articles/PMC...

No evidence that plasmablasts transdifferentiate into developing neutrophils in severe COVID‐19 disease

A recent single‐cell RNA sequencing study by Wilk et al. suggested that plasmablasts can transdifferentiate into ‘developing neutrophils’ in patients with severe COVID‐19 disease. We explore the evide...

pmc.ncbi.nlm.nih.gov

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Jeff Mold @jeffmold.bsky.social · 1d

I wish the journals would start retracting or putting warning s on all the fast tracked covid papers that were wrong… starting with the plasma cell transmogrification into neutrophils or vice versa one: pubmed.ncbi.nlm.nih.gov/32514174/ Cited 1600x!?!?

A single-cell atlas of the peripheral immune response in patients with severe COVID-19 - PubMed

There is an urgent need to better understand the pathophysiology of Coronavirus disease 2019 (COVID-19), the global pandemic caused by SARS-CoV-2, which has infected more than three million people wor...

pubmed.ncbi.nlm.nih.gov

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Jeff Mold @jeffmold.bsky.social · 1d

For me it’s this paper that started the ridiculous “covid is like hiv” insanity. And then a pile on by uninformed people on social media misunderstanding how T cells relocate during acute inflammatory responses… I’ll make a point of clearly teaching this to my students this fall

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Jeff Mold @jeffmold.bsky.social · 1d

One more in a growing number of irresponsible publications which use “big data” to try and look for any signs of an effect and then market it like hell for cites/impact

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Jeff Mold @jeffmold.bsky.social · 1d

It’s insane how one crappy nature immunology paper and efforts to spin a narrative to increase impact can have so much damage… or at least I credit it to that “il7r- naive” T cells are depleted hogwash

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Jeff Mold @jeffmold.bsky.social · 1d

I think it’s given by the Norwegians… but I highly doubt Trump knows that or the area codes of either country

Jeff Mold @jeffmold.bsky.social · 2d

Love your work. It’s inspiring!

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Reposted by Jeff Mold

Inigo Martincorena @imartincorena.bsky.social · 2d

Our latest work is out in Nature today. In this paper, we introduce an improved version of NanoSeq, a duplex sequencing protocol with <5 errors per billion bp in single DNA molecules, and use it to study the somatic mutation landscape of oral epithelium in >1000 people www.nature.com/articles/s41...

Somatic mutation and selection at population scale - Nature

A new version of nanorate DNA sequencing, with an error rate lower than five errors per billion base pairs and compatible with whole-exome and targeted capture, enables epidemiological-scale studies of somatic mutation and selection and the generation of high-resolution selection maps across coding and non-coding sites for many genes.

www.nature.com

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Jeff Mold @jeffmold.bsky.social · 2d

ohhhhhhhh wow
www.nature.com/articles/s41...

Somatic mutation and selection at population scale - Nature

A new version of nanorate DNA sequencing, with an error rate lower than five errors per billion base pairs and compatible with whole-exome and targeted capture, enables epidemiological-scale studies of somatic mutation and selection and the generation of high-resolution selection maps across coding and non-coding sites for many genes.

www.nature.com

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Reposted by Jeff Mold

Ryan Flynn @raflynn5.bsky.social · 3d

We’re excited to report work led by postdoc Jennifer Porat in the lab, finding that DNA accumulates on the surface of living cells and that the secreted extracellular protein DNASE1L3 can modulate its levels on B and T cells. With a new twist for ATAC-seq as well www.biorxiv.org/content/10.1...

DNASE1L3 surveils mitochondrial DNA on the surface of distinct mammalian cells

The extracellular space is a critical environment for discriminating self versus non-self nucleic acids and initiating the appropriate immune responses through signaling cascades to relay information ...

www.biorxiv.org

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Jeff Mold @jeffmold.bsky.social · 3d

Homo sapiens?

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Jeff Mold @jeffmold.bsky.social · 4d

Ah of course shevach!

Jeff Mold @jeffmold.bsky.social · 4d

I always associated Wildin with the scurfy story too

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Jeff Mold @jeffmold.bsky.social · 4d

I guess the focus was on foxp3 or else one could’ve included Maria Grazia Roncarolo and it’s a shame rudensky was left off since he was right there on foxp3 huh

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Jeff Mold @jeffmold.bsky.social · 4d

I’m just a big fan of his early work and perseverance to study something everyone else had given up on is all :)

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Jeff Mold @jeffmold.bsky.social · 4d

Love Sakaguchi for Nobel! pubmed.ncbi.nlm.nih.gov/7636184/

Immunologic self-tolerance maintained by activated T cells expressing IL-2 receptor alpha-chains (CD25). Breakdown of a single mechanism of self-tolerance causes various autoimmune diseases - PubMed

Approximately 10% of peripheral CD4+ cells and less than 1% of CD8+ cells in normal unimmunized adult mice express the IL-2 receptor alpha-chain (CD25) molecules. When CD4+ cell suspensions prepared f...

pubmed.ncbi.nlm.nih.gov

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Reposted by Jeff Mold

Simon Fisher @profsimonfisher.bsky.social · 6d

Twenty-four years ago today, our paper “A forkhead-domain gene is mutated in a severe speech and language disorder” was published: www.nature.com/articles/350....
A personal thread about the ups & downs of the journey we took to get to that point....1/n
🗣️🧬🧪

Image shows the first two printed pages of the paper “A forkhead-domain gene is mutated in a severe speech and language disorder” by Cecilia Lai and colleagues, published in Nature in 2001 (volume 413, pages 519-523). The abstract reads as follows:
Individuals affected with developmental disorders of speech and language have substantial difficulty acquiring expressive and/or receptive language in the absence of any profound sensory or neurological impairment and despite adequate intelligence and opportunity. Although studies of twins consistently indicate that a significant genetic component is involved, most families segregating speech and language deficits show complex patterns of inheritance, and a gene that predisposes individuals to such disorders has not been identified. We have studied a unique three-generation pedigree, KE, in which a severe speech and language disorder is transmitted as an autosomal-dominant monogenic trait. Our previous work mapped the locus responsible, SPCH1, to a 5.6-cM interval of region 7q31 on chromosome 7. We also identified an unrelated individual, CS, in whom speech and language impairment is associated with a chromosomal translocation involving the SPCH1 interval. Here we show that the gene FOXP2, which encodes a putative transcription factor containing a polyglutamine tract and a forkhead DNA-binding domain, is directly disrupted by the translocation breakpoint in CS. In addition, we identify a point mutation in affected members of the KE family that alters an invariant amino-acid residue in the forkhead domain. Our findings suggest that FOXP2 is involved in the developmental process that culminates in speech and language.

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Reposted by Jeff Mold

bioRxivpreprint @biorxivpreprint.bsky.social · 6d

Segregating DNA lesions point to high selective advantage of tumor initiating cells https://www.biorxiv.org/content/10.1101/2025.10.02.680094v1

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Reposted by Jeff Mold

Ed Zitron @edzitron.com · 9d

Here’s part 3 of our four part Better Offline case against generative AI. I walk you through how “AI replacing software engineers” is a myth - and how Microsoft only has 8 million active paying customers for Microsoft 365’s AI Copilot.

podcasts.apple.com/us/podcast/b...
Linktr.ee/betteroffline

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Jeff Mold @jeffmold.bsky.social · 9d

I’ve really enjoyed these. Keep up the good work

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Jeff Mold @jeffmold.bsky.social · 10d

What about fat commander in chiefs?

edition.cnn.com/2025/09/30/p...

Hegseth criticizes ‘fat troops’ and ‘fat generals’ | CNN Politics

Defense Secretary Pete Hegseth told top military officers that he no longer wants to see “fat generals and admirals” or overweight troops in combat formations. Hegseth emphasized the importance of new...

edition.cnn.com

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Jeff Mold @jeffmold.bsky.social · 11d

Huh, pDCs... what are they good for then, absolutely nothing? www.nature.com/articles/s41...

Plasmacytoid dendritic cells are dispensable or detrimental in murine systemic or respiratory viral infections - Nature Immunology

Previous research has suggested that pDCs are required for an effective antiviral immune response, but direct experimental evidence to support this is lacking. Here Ngo et al. develop a pDC knockin mouse model and find that pDCs are dispensable for an antiviral immune response to mouse cytomegalovirus and may be detrimental during influenza or SARS-CoV-2 infection.

www.nature.com

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Reposted by Jeff Mold

Edouard Hannezo @ehannezo.bsky.social · Dec 17

Happy to share the latest work from Preeti Sahu, with Adriana Sanchez-Danes on the biomechanics of cell fate choices during tumor initiation! We implement/test a 3D vertex model with proliferation and fate choices for multilayered tissues! See 🧵 below (1/n) bit.ly/3ZXxJzk

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