Indeed, KIN-20 exhibits dynamic localization to the nucleus – dependent on LIN-42 binding. We speculate that this may provide KIN-20 to access to additional substrates. 6/n

Animals lacking CK1/KIN-20 or its enzymatic activity are highly arrhythmic – in fact much more so than animals only lacking the LIN-42_CK1BD. This made us wonder whether the key function of the complex is regulation of KIN-20 by LIN-42, rather than the other way around. 5/n

LIN-42 co-immunoprecipitates KIN-20 – an orthologue of Casein Kinase 1delta/epsilon that also occurs in a complex with PER in mammals. The LT/SYQ region forms a CK1-binding domain (CK1BD) that also regulates CK1 activity. CK1 phosphorylates LIN-42. 4/n

And the next one: dx.doi.org/10.1038/s44318-025-00585-z . Super-fun collaboration with @partchlab.bsky.social & @gotworms.bsky.social to find similarities between developmental and circadian clocks – supported by @fmiscience.bsky.social Facilities and, financially, @snsf.ch and @erc.europa.eu . 1/n

We validated the model experimentally, by acutely depleting GRH-1. The model reliably predicted the resulting changes in chromatin opening, even in those cases where they were not caused by GRH-1 directly, but, indirectly, through GRH-1’s effect on other TFS. 9/n

In an extreme case, such additive activity can lead to a phenomenon of “destructive interference”, where the rhythmic activities of different TFs cancel each other out to cause non-rhythmic chromatin opening. 8/n

Using a model with only these 9 TFs, and considering their binding strengths, we could predict chromatin dynamics of any phase and amplitude. Since we used linear models without interaction terms, this reveals that new phases and amplitudes can be generated by adding up the activity of TFs. 7/n

So then what generates these broad peak phase dispersion? Knowing that oscillations are transcriptional, we went to identify regulatory elements through an ATAC-seq timecourse. Strikingly, we saw extensive rhythmic opening and closing of chromatin – again with broad peak phase dispersion. 4/n

So we did scRNA-seq at different time points during a larval stage - and found oscillations in 7 epithelial tissues. Yet, these each had a broad peak phase dispersion. Moreover, most genes were predominantly expressed in only one of the tissues. 3/n

This was the starting point doi.org/10.15252/msb... 1000s of "oscillating" genes, all peaking once per larval stage, but at different times. How is this broad dispersion of peak phases achieved? Perhaps a superposition of different tissues, given that the observation was with whole animal data? 2/n

Paper alert! doi.org/10.1038/s443... - "A scheduler for rhythmic gene expression". We show how 9 txn factors suffice for rhythmic gene expression of thousands of genes with any phase or amplitude in #Celegans larvae (and also look at the tissues where oscillations happen) 1/n

And now, hopefully, with properly displayed figure (looked fine in the preview before...)

Not all artifact, but very prone to artifact, no matter the number of replicates (e.g., if your strains develop at different speeds). We discussed some sanity checks and approaches here: doi.org/10.1016/bs.c.... Ideally, do time courses, but minimally check compuationally for evidence of mistiming.

Happy to announce that @labgrosshans.bsky.social is now on Bluesky. We care about bluesky research - specifically on biological clocks. At the FMI in Basel, Switzerland, we combine experiment, computational analysis and theoretical approaches to understand how organisms time development.