ArticleThe EMBO journal2026
Single-nucleotide m⁶A mapping uncovers redundant YTHDF function in planarian progenitor fate selection.
Article in The EMBO journal, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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.
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.
Who cites it
2 citing papers in PubMed.
- The stability of m6A-marked transcripts is linked to cell identity in planarians.Nucleic acids research · 2026Article
- NResearch (Washington, D.C.) · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
Abstract
Cell fate decisions require tight regulation of gene expression. In planarians, highly regenerative flatworms, the mRNA modification N⁶-methyladenosine (m⁶A) modulates progenitor production and fate. However, the mechanisms governing m⁶A deposition in the planarian transcriptome, and the role of their expanded family of YTHDF m⁶A reader proteins in orchestrating biological functions, remain unclear. Here, we generated the first single-nucleotide resolution map of m⁶A in planarians, and revealed that simple sequence rules guide m⁶A deposition, facilitating the flexible evolutionary gain and loss of these marks. Functional analyses of the five YTHDF planarian m⁶A readers revealed that while individual reader expression is dispensable, together, the planarian YTHDF proteins regulate the production of specific progenitor lineages and overall body size. Collectively, our findings uncover a robust, redundant regulatory architecture for cell fate control in planarians, characterized by multiple m⁶A sites per gene and coordinated m⁶A reader expression. This architecture is essential for proper lineage resolution and provides insights into the evolutionary dynamics of the m⁶A landscape.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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 OpenQuestion graph.