Our BioRxiv preprint on CTCF's target search mechanism is now published in Nature Chemical Biology:

• We show that CTCF exhibits anisotropic diffusion
• We devise the Anisotropic Diffusion through transient Trapping in Zones model (ADTZ-model) to theoretically explain the data
• We show that the zones likely correspond to CTCF clusters
• Deleting the internal RNA-Binding Region (RBRi) in CTCF strongly reduces both trapping and CTCF clustering

Shdema Filler-Hayut is joining the lab as a post-doc starting in early 2020. Shdema is joining the lab from the Weizmann Institute in Israel, where she worked with Avraham Levy on how double-strand breaks (DSBs) are repaired in plants. In particular, Shdema showed that DSBs in somatic plant cells can be repaired using homologous chromosomes by exploiting Cas9 and a clever genetic approach in tomatoes, with deeps applications for improving agriculture.
We are thrilled that Shdema is joining the lab and look forward to welcoming her. 

Our preprint describing our functional characterization of an internal RNA-Binding Region (RBRi) in CTCF is online today in Molecular Cell.

• We show that CTCF self-associates in a largely RNA-dependent and DNA-independent manner
  
• When we delete the RBRi in CTCF endogenously in mESCs, the cells get very sick, suggesting its functional important.
  
• RBRi-del-CTCF shows substantially lower clustering in cells
  
• RBRi-del-mESCs have lost about 1/3-1/2 of all chromatin loops
  
• CTCF binding sites and CTCF loops fall into at least 2 distinct classes: RBRi-dependent or RBRi-independent
  

Overall, we believe our discovery of distinct classes of chromatin loops highlights a key future question: what are the mechanistic differences between these sites?
Also check out a similar story published back-to-back.

Michele Gabriele is joining the lab as a post-doc starting in early 2020. Michele is joining the lab from SEMM - the European School of Molecular Medicine - at the University of Milan, where he worked with Giuseppe Testa on modeling human neurodevelopmental disorders caused by mutations in genes related to chromatin and regulation of gene expression using patient-derived cells.
One of his papers - how YY1 haploinsufficiency can cause intellectual disability - recently resulted in OMIM naming the disease after him: Gabriele-de Vries Syndrome.
We are delighted to have Michele join the lab

Our preprint reporting the absolute quantification of CTCF (~217k proteins per cell) of cohesin (through Rad21; ~109k proteins per cell) in mouse embryonic stem cells has now been published in eLife.
We use these measurements to estimate constraints on models of 3D genome organization: the time-averaged occupancy of an average CTCF binding site is ~50% and the density of putatively loop extruding cohesins is 5.3 per Mb (if monomeric).
We also present biochemical evidence for cohesin-cohesin interactions and we report a very simple, convenient and easy method for absolute abundance quantification of any Halo-tagged protein of interest.
The full paper is here: https://elifesciences.org/articles/40164
And a back-to-back complementary paper in HeLa cells is here: https://elifesciences.org/articles/46269

We just posted a new preprint "Promoters adopt distinct dynamic manifestations depending on transcription factor context".
Find it here: https://www.biorxiv.org/content/10.1101/650762v2
In this work with Christoph Zechner, we study how promoters responds to different patterns of dynamic transcription factor input in budding yeast. Surprisingly, we find that promoters can exhibit qualitatively distinct scaling behaviors depending on TF input. We refer to this observation as context dependent "manifestations".

New preprint from Stanley Hsieh. Using Micro-C to generate 3D contact maps of mouse embryonic stem cells, we see a whole new level of genome organization below the levels of TADs.
This includes enhancer-enhancer, promoter-promoter and enhancer-promoter interactions and stripes/flames. We also find a new type of small domains. We call these microTADs.
Moreover, it seems like besides CTCF/Cohesin, these microTADs are often demarcated by the transcriptional machinery.
Read the full story here on BioRxiv.

And see also a back-to-back preprint from Oliver Rando's lab with the Mirny and Dekker labs on BioRxiv.