Selected publication milestones, not an exhaustive history or discovery priority claim.
2008 — 2008:local upstream ncRNA transcription is required for fbp1 chromatin opening in fission yeast, demonstrating a reverse-direction route. Original PMID18820678.
2015 — 2015:targeted p300 acetyltransferase activates endogenous genes; artificial acetylation/coactivator recruitment is separated from opening alone. Original PMID25849900.
2017 — 2017:OCT4 requires BRG1 for selected regulatory-element function in mouseESCs, mapping pioneer/remodeler cooperation. Original PMID28287392.
2019 — 2019:repli-ATAC and transcription inhibition show transcription restart contributes to postreplication accessibility restoration. Original PMID31126739.
2020 — 2020:early zebrafish opening precedes activation and largely survives transcription inhibition, with miR430 as an exception. Original PMID31940339.
2021 — 2021:acute BAF degradation/ATPase inhibition identifies minute-scale accessibility maintenance; early transcription effects and tag baselines require separate interpretation. Original PMID33558760.
2022 — 2022:targeted active/dead HAT contrasts show opening alone can fail to activate an endogenous target during ZGA. Original PMID35182480.
2023 — 2023:EP400 compensation restores many promoter states/outputs; paused-polymerase/BAF work published2024(PMID38049663) strengthens bidirectional cooperation. Original PMID37922899.
2025 — 2025:BRG1 dose manipulation shows enhancer sensitivity and buffered transcription, refining a simple one-to-one access model. Original PMID40846763.
2026 — 2026:single-fiber nucleosome-distortion and factor-domain experiments refine the physical meaning of molecular DNA access. Original PMID42056506.
A selective accessible-state necessity intervention must preserve the multifunctional regulators that establish it.
Competence requires a standardized activating challenge and cannot be inferred from either basal ATAC or basal RNA alone.
Bulk ATAC/DNase, methylase footprinting, local nucleosome distortion and large-scale decondensation measure different aspects of access.
Temporal direction depends on developmental, replication and stimulus context; a universal upstream or downstream account fails.
Specificity of factor/remodeler perturbations must exclude cell-cycle, viability, replication stress and transcriptional-collapse alternatives at each sampled time.
Opening-only sufficiency fails at named loci, while acetylation/coactivator rescue can work; these need independent locus/state replication.
Preprint/update duplication, shared reagents and repeated loci must be distinguished from independent error classes.
At prespecified native promoters/enhancers, alter DNA accessibility with an orthogonal state intervention while preserving factor occupancy, activation domains, acetylation/coactivators and polymerase function as far as possible. Apply a matched activating stimulus and measure initiation/bursting with calibrated nascent RNA and single-fiber accessibility. Restore only the accessible state in a matched rescue; retain a dead-HAT opening-without-activation control. Verify cell-cycle distribution, replication stress, viability, target-factor abundance and local cis sequence across developmental/replication windows.