Pietro Pichierri

@pietropichierri.bsky.social

Among other things, a scientist trying to understand how cells avoid things going wrong during DNA replication. http://www.genomestabilitygroup.com/

Great to see this out in it's final form. To interpret the results from a CDC7i CRISPR screen, Bernard used DepMap co-essentiality to group all hits into functional clusters, identifying CDK8 in a DNA replication group. It's a nice way to quickly get from hit lists to interpretable pathway groupings

The EMBO Journal@embojournal.org · 3d ago

Surprising non-transcriptional function for mediator kinase CDK8 in human DNA replication: Corrado Santocanale & coworkers find it to cooperate with CDC7 in MCM helicase phosphorylation & activation–with implications for antiproliferative actions of CDC7 inhibitors link.springer.com/article/10.1...

1\ We know a bit about how 3D chromatin interactions are formed, but what do we know about how they are disrupted? We asked this question in our latest preprint: doi.org/10.64898/202..., focusing on the massive loss of promoter interactions during neuronal differentiation.

Developmentally programmed loss of long-range Polycomb interactions is regulated by cohesin

Distal regulatory elements (DREs), such as enhancers, can regulate genes across megabase-long distances, presumably via coming into close spatial proximity. The establishment of new transcriptional programmes during cell type transitions is associated with widespread rewiring of the spatial organisation of the genome, including gain and loss of chromatin interactions. Extensive effort has been invested into understanding how chromatin interactions are formed during development, yet the mechanisms underlying their developmental loss remain largely unclear. By leveraging chromatin accessibility-assisted footprinting, acute protein degradation and chromatin conformation capture, we show that loss of promoter interactions cannot be explained by reduced binding of sequence-specific transcription factors (TFs). Instead, we identify a subset of interactions that depend on cohesin for programmed developmental disruption. These sites are characterized by high Polycomb enrichment and TF occupancy and engage in strong long-range interactions that undergo extensive differentiation-dependent rewiring. Preventing interaction loss by acute cohesin degradation results in the preferential downregulation of associated genes. Together, these results suggest that cohesin indirectly regulates developmental loss of Polycomb interactions by enabling the acquisition of other potentially regulatory contacts in a process that may shape transcriptional programs during cell type transitions. ### Competing Interest Statement The authors have declared no competing interest. European Research Council Helmholtz Society, VH-NG-1604

doi.org

I know I am repeating myself here but: in 2012 the right-wing government did this in Spain. They dismantled the Ministry of Science and incorporated it as a department in the Ministry of Economy. This effectively gave them control over the entire budget because it was one and the same 🧪

Nature@nature.com · 2mo ago

An agreement paves the way for hundreds of millions of dollars’ worth of projects to be transferred from the NIH’s institute for infectious diseases to the Department of Defense. go.nature.com/4ycEbk8

CRISPR-based experiments build a more complete picture of the regulation of interferon responses, which may inform the development of treatments for immunodeficiencies or inflammatory disorders linked to aberrant IFN production. #ScienceSignaling https://scim.ag/4qth02y

A genome-wide map of the genetic network in monocytes that regulates type I interferon induction by the cGAS-STING pathway

Genetic screens identify context-dependent regulators of STING-driven IFN-β induction in monocytes.

scim.ag

Happy to share a brand new story from the group! Started in 2019, stopped for pandemic and revived in 2025. Kudos to all authors and especially to Benedetta and Floriana who is taking the challenge! Take-home message: even small deviations from the norm can make big changes in life... Stay tuned!

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bioRxiv Cell Biology@biorxiv-cellbio.bsky.social · 3mo ago

Subthreshold perturbation of DNA replication induces a secretory response and a bystander effect in naïve human fibroblasts https://www.biorxiv.org/content/10.64898/2026.08.20.745990v1

I just completed my standing study section service in June (2022-2026) and want to emphasize Bryan's point: maintaining the integrity of the peer review process is an important act of service for our colleagues, especially right now. If you are asked and can swing it, please consider serving.

BWJones@bwjones.bsky.social · 3mo ago

Just accepted the 2nd study section invitation for this autumn/winter. If you can serve on study section, please accept when asked. The SROs and the POs are working so hard to get good science funded.

Bastano poche righe a descrivere responsabilmente la realtà dei fatti a Ceuta. Ma i sovranisti scatenano l’indegna cagnara dell’invasione, minano la solidarietà europea e speculano sui morti.

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A simple but (I think) compelling re-analysis of a paper that Director Bhattacharya frequently cites in his talks to claim that NIH-funded researchers no longer pick up the newest ideas. Dr. Bishop concludes the opposite using the same data. The original conclusion was contrary to my experience.

Dorothy Bishop@deevybee.bsky.social · 3mo ago

Further analysis of Packalen & Bhattacharya article, where they claimed #NIH-funded research was slow to pick up on new ideas. I argue that their approach is flawed, and I present an analysis that shows the exact opposite. pubpeer.com/publications...

“Once again, the answer to critique and demands to ‘reform‘ the NIH is a simple ‘they already do that’...The next response is ‘if you want more of this thing they already do, than give the NIH an increase in budget. Otherwise, what specific core activities of the NIH are to be cut to pay for that?’”

Drug Monkey@drugmonkey.bsky.social · 4mo ago

NIH must "open scientific careers to skilled craftspeople and practitioners" drugmonkey.wordpress.com/2026/07/22/n...

Study (N=8,097) finds women more likely to finish a PhD before 30 & have children after 35. Men tended to become parents during doctoral studies & often had 3+ children by 40. Early-career mothers had lower citation rates; fathers had no such penalties. www.insidehighered.com/news/faculty...

Female Academics Increasingly Delay Motherhood Until Age 35

“Pronounced penalties” for those early-career staff with children may explain why Ph.D.s postpone becoming parents, a recent study finds.

insidehighered.com

NIH grants have been under political scrutiny since early 2025. But what does the screening process actually look like? What is being flagged? I spent a month digging into leaked docs and emails. We've published the 235-word list that are being flagged by an internal AI tool. And so much more. 🧵

Inside the new political screening that’s stalling NIH grants

Mandatory reviews by top health officials and checks for 235 disfavoured terms have left hundreds of vetted grant applications in administrative limbo.

nature.com

I for one like the idea of limiting the number of R01 type grants a lab can have to help diversify the research being done. However, the data (a little out of date) says this is not the problem. The issue is ever decreasing $ to the NIH in inflationary dollars.

Drug Monkey@drugmonkey.bsky.social · 5mo ago

Talk of limiting grants, by number or by dollars, should be informed by data. It’s been a long time since we got NIH information on grants per PI. drugmonkey.scientopia.org/2013/01/30/p...

Here is our article published in Nature Comm, on new players in chromatin dynamics after UV repair. This work highlights the histone chaperones DNAJC9 and MCM2 as central players in chromatin repair. Our proteomic dataset opens up new perspectives for dissecting epigenome maintenance mechanisms.

Proteomic profiling of UV damage repair patches uncovers histone chaperones with central functions in chromatin repair - Nature Communications

Chromatin states need to be maintained during DNA damage repair. Here, the authors expand the histone chaperone network involved in repair-coupled chromatin restoration and highlight a mechanistic coo...

nature.com