Genome-wide chromatin reset at the onset of leg regeneration in pancrustaceans
- 1Institute for Advanced Biosciences - INSERM - CNRS - UGA
Abstract
Regeneration requires injured tissues to selectively reactivate certain developmental programs while triggering regeneration-specific mechanisms and responding to the immediate consequences of tissue damage. How chromatin states are reorganized during this transition, and whether the underlying sequence of regulatory events is conserved across regenerating animals, remain poorly understood. We address these questions in the two-spotted cricket Gryllus bimaculatus, in which limb regeneration progressively declines during nymphal development and is absent in adults, and extend our analysis to the crustacean Parhyale hawaiensis. We first establish a chromosome-scale genomic and epigenomic framework for the cricket and then follow chromatin and transcriptional changes after limb amputation. Amputation triggers a striking genome-wide shutdown of enhancer-associated chromatin, marked by loss of accessible regulatory regions and depletion of H3K27ac and H3K4me1. This is followed, in regeneration-competent tissue, by selective reopening of a restricted population of regulatory elements and strong induction of the pioneer transcription factor Zelda (GbZelda). The GbZelda locus is unusually marked by both H3K27me3 and H3K9me3 in intact leg tissue; after injury, H3K9me3 is reduced broadly, whereas H3K27me3 is selectively relieved in regenerating nymphs. Finally, analysis of Parhyale reveals the same sequence of chromatin events during appendage regeneration: an initial enhancer shutdown followed by selective regulatory reopening concomitant with Zelda upregulation. Thus, rather than restoring the pre-injury regulatory landscape wholesale, appendage regeneration in these two pancrustacean models proceeds through a conserved sequence of genome-wide chromatin resetting, selective regulatory reopening and activation of a pioneer transcription factor.
Related
- isl1a coordinates onset and termination of regeneration of the zebrafish lateral line
- Genome-wide loss of chromatin accessibility coexists with selectively elevated RNA abundance in nutrient-starved U2OS cells
- DNA damage at Lamina-Associated Domains triggers nuclear envelope reorganization and chromatin detachment to prevent nuclear envelope blebbing and genome instability.
- Localized Chromatin Rewiring Shapes Rhythmic Transcription within a Stable 3D Genome in Rice
- Local chromatin, 3D genome folding and transposon cargo shape Sleeping Beauty transposition
BibTeX
@misc{louvier2026genomewide,
title = {{Genome-wide chromatin reset at the onset of leg regeneration in pancrustaceans}},
author = {M. Louvier and G. Forbes and M. Mohammed-Ali and E. Moutaux and F. Chuffart and A. Argoud and F. Girard and A. Dumont and B. Pachano and C. Swale and M.-A. Hakimi and R. Koszul and A. Piazza and M. Averof and M. Paris and G. A. Orsi},
howpublished = {bioRxiv},
year = {2026},
month = oct,
doi = {10.64898/2026.10.09.757970},
url = {https://www.biorxiv.org/content/10.64898/2026.10.09.757970v1},
note = {CC BY},
}
RIS
TY - UNPB
TI - Genome-wide chromatin reset at the onset of leg regeneration in pancrustaceans
AU - M. Louvier
AU - G. Forbes
AU - M. Mohammed-Ali
AU - E. Moutaux
AU - F. Chuffart
AU - A. Argoud
AU - F. Girard
AU - A. Dumont
AU - B. Pachano
AU - C. Swale
AU - M.-A. Hakimi
AU - R. Koszul
AU - A. Piazza
AU - M. Averof
AU - M. Paris
AU - G. A. Orsi
PY - 2026
DA - 2026/10/09
PB - bioRxiv
DO - 10.64898/2026.10.09.757970
UR - https://www.biorxiv.org/content/10.64898/2026.10.09.757970v1
AB - Regeneration requires injured tissues to selectively reactivate certain developmental programs while triggering regeneration-specific mechanisms and responding to the immediate consequences of tissue damage. How chromatin states are reorganized during this transition, and whether the underlying sequence of regulatory events is conserved across regenerating animals, remain poorly understood. We address these questions in the two-spotted cricket Gryllus bimaculatus, in which limb regeneration progressively declines during nymphal development and is absent in adults, and extend our analysis to the crustacean Parhyale hawaiensis. We first establish a chromosome-scale genomic and epigenomic framework for the cricket and then follow chromatin and transcriptional changes after limb amputation. Amputation triggers a striking genome-wide shutdown of enhancer-associated chromatin, marked by loss of accessible regulatory regions and depletion of H3K27ac and H3K4me1. This is followed, in regeneration-competent tissue, by selective reopening of a restricted population of regulatory elements and strong induction of the pioneer transcription factor Zelda (GbZelda). The GbZelda locus is unusually marked by both H3K27me3 and H3K9me3 in intact leg tissue; after injury, H3K9me3 is reduced broadly, whereas H3K27me3 is selectively relieved in regenerating nymphs. Finally, analysis of Parhyale reveals the same sequence of chromatin events during appendage regeneration: an initial enhancer shutdown followed by selective regulatory reopening concomitant with Zelda upregulation. Thus, rather than restoring the pre-injury regulatory landscape wholesale, appendage regeneration in these two pancrustacean models proceeds through a conserved sequence of genome-wide chromatin resetting, selective regulatory reopening and activation of a pioneer transcription factor.
ER -