Evidence map›Paper›PMID 42119979›Full record

ArticleThe Journal of biological chemistry2026

TIP60 acts as a wound-induced factor essential for efficient regeneration in planaria.

Akansha Pal, Ankit Arora, Hemant Kumar, Anna Thokchom, Bharti Jaiswal, Dasaradhi Palakodeti, Ashish Gupta

Abstract read
In one paragraph

Article in The Journal of biological chemistry, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors.

Akansha PalCenter of Excellence in Epigenetics, Department of Life Sciences, Shiv Nadar Institution of Eminence, Greater Noida, Uttar Pradesh, India.
Ankit AroraChemical Biology Approaches for Stem Cells and Therapeutics (ICB), Institute for Stem Cell Science and Regenerative Medicine (inStem), Bengaluru, India.
Hemant KumarCenter of Excellence in Epigenetics, Department of Life Sciences, Shiv Nadar Institution of Eminence, Greater Noida, Uttar Pradesh, India.
Anna ThokchomCenter of Excellence in Epigenetics, Department of Life Sciences, Shiv Nadar Institution of Eminence, Greater Noida, Uttar Pradesh, India.
Bharti JaiswalChemical Biology Approaches for Stem Cells and Therapeutics (ICB), Institute for Stem Cell Science and Regenerative Medicine (inStem), Bengaluru, India.
Dasaradhi PalakodetiChemical Biology Approaches for Stem Cells and Therapeutics (ICB), Institute for Stem Cell Science and Regenerative Medicine (inStem), Bengaluru, India. Electronic address: dasaradhip@instem.res.in.
Ashish GuptaCenter of Excellence in Epigenetics, Department of Life Sciences, Shiv Nadar Institution of Eminence, Greater Noida, Uttar Pradesh, India. Electronic address: ag315@snu.edu.in.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chromatin modifiers regulate genome function by modulating chromatin structure and are essential for processes such as transcription, DNA repair, and cell division. The lysine acetyltransferase TIP60 (KAT5), a member of the MYST family, is a key regulator of chromatin dynamics and has established roles in stem cell maintenance and differentiation, however its function in regeneration remains unclear. Here, we investigated the role of the TIP60 homolog (SMED-TIP60) in the planarian Schmidtea mediterranea, a model system for stem cell-driven regeneration. Biochemical analyses demonstrated that SMED-TIP60 possesses both histone acetyltransferase and autoacetylation activities. Functional depletion of Smed-tip60 by RNA interference impaired tissue homeostasis and survival. Regeneration assays revealed severe defects in blastema formation, culminating in a complete failure of regeneration upon TIP60 loss. Mechanistically, in situ hybridization and immunofluorescence analyses showed a marked reduction in stem cell populations and proliferation in Smed-tip60 RNAi animals. Injury-induced expression of SMED-TIP60 peaked at 5 days post-amputation, and transcriptomic (RNA-seq) analysis revealed widespread dysregulation of gene expression at both anterior and posterior wound sites, with increased transcriptional perturbation correlating with elevated TIP60 levels. Furthermore, key wound-response genes were aberrantly expressed in Smed-tip60-depleted animals, indicating disruption of the injury-response program and positional information resetting. Collectively, these findings identify TIP60 as an essential regulator of stem cell-mediated regeneration, functioning to coordinate wound-response gene expression and tissue restoration.

Indexed as

Lysine Acetyltransferase 5PlanariansRegenerationAnimalsRNA InterferenceLysine Acetyltransferase 5blastemacell proliferationchromatin modifierneoblast cellsplanaria regenerationTIP60wound induced genes

Identifiers

PMID42119979
PMCPMC13264050

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.