FAIR sharing of Chromatin Tracing datasets using the newly developed 4DN FISH Omics Format.

A key output of the NIH-Common Fund 4D Nucleome (4DN) project is the open publication of datasets related to the structure of the human cell nucleus and the genome. Recent years have seen a rapid expansion of multiplexed Fluorescence In Situ Hybridization (FISH) or FISH-omics methods, which quantify the spatial organization of chromatin in single cells, sometimes together with RNA and protein measurements, and provide an expanded understanding of how 3D higher-order chromosome structure relates to transcriptional activity and cell development in both health and disease. Despite this progress, results from Chromatin Tracing FISH-omics experiments are difficult to share, reuse, and subject to third-party downstream analysis due to the lack of standard specifications for data exchange.

Distinct signaling signatures drive compensatory proliferation via S-phase acceleration.

Regeneration relies on cell proliferation to restore damaged tissues. Multiple signaling pathways activated by local or paracrine cues have been identified to promote regenerative proliferation. How different types of tissue damage may activate distinct signaling pathways and how these differences converge on regenerative proliferation is less well defined.

The 4D Nucleome Data Portal as a resource for searching and visualizing curated nucleomics data.

The 4D Nucleome (4DN) Network aims to elucidate the complex structure and organization of chromosomes in the nucleus and the impact of their disruption in disease biology. We present the 4DN Data Portal ( https://data.4dnucleome.

Micro-Meta App: an interactive tool for collecting microscopy metadata based on community specifications.

For quality, interpretation, reproducibility and sharing value, microscopy images should be accompanied by detailed descriptions of the conditions that were used to produce them. Micro-Meta App is an intuitive, highly interoperable, open-source software tool that was developed in the context of the 4D Nucleome (4DN) consortium and is designed to facilitate the extraction and collection of relevant microscopy metadata as specified by the recent 4DN-BINA-OME tiered-system of Microscopy Metadata specifications. In addition to substantially lowering the burden of quality assurance, the visual nature of Micro-Meta App makes it particularly suited for training purposes.

JNK-dependent cell cycle stalling in G2 promotes survival and senescence-like phenotypes in tissue stress.

The restoration of homeostasis after tissue damage relies on proper spatial-temporal control of damage-induced apoptosis and compensatory proliferation. In imaginal discs these processes are coordinated by the stress response pathway JNK. We demonstrate that JNK signaling induces a dose-dependent extension of G2 in tissue damage and tumors, resulting in either transient stalling or a prolonged but reversible cell cycle arrest.

Correction to: DamID profiling of dynamic Polycomb-binding sites in Drosophila imaginal disc development and tumorigenesis.

Unfortunately, the original version of this article contained a typographical error in one of the author names. The name of the author Alexey Pindyurin was incorrectly spelt as Alexey Pinduyrin. The correct spelling is included here and has been updated in the original article.

DamID profiling of dynamic Polycomb-binding sites in Drosophila imaginal disc development and tumorigenesis.

Background: Tracking dynamic protein-chromatin interactions in vivo is key to unravel transcriptional and epigenetic transitions in development and disease. However, limited availability and heterogeneous tissue composition of in vivo source material impose challenges on many experimental approaches.

Results: Here we adapt cell-type-specific DamID-seq profiling for use in Drosophila imaginal discs and make FLP/FRT-based induction accessible to GAL driver-mediated targeting of specific cell lineages.

JAK/STAT signalling mediates cell survival in response to tissue stress.

Tissue homeostasis relies on the ability of tissues to respond to stress. Tissue regeneration and tumour models in Drosophila have shown that c-Jun amino-terminal kinase (JNK) acts as a prominent stress-response pathway promoting injury-induced apoptosis and compensatory proliferation. A central question remaining unanswered is how both responses are balanced by activation of a single pathway.