ArticlePLoS genetics2026
The rewiring of a terminal selector regulatory cascade generates convergent neuronal laterality.
Article in PLoS genetics, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- Paralog-specific miRNA regulation uncouples ASER gene repression from the canonicalmicroPublication biology · 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
6 authors.
Funding
Abstract
Neuronal identity is established and maintained by "terminal-selector" transcription factors, yet how these networks evolve remains unclear. We examined the specification of the chemosensory ASE and thermosensory AFD neurons in the nematode Pristionchus pacificus, a species that expresses the terminal-selector, Ppa-CHE-1, in both sensory neurons. To determine if the ASE neurons exhibit left-right laterality, we used HCR-FISH and transgenic reporters to discover 8 ASE left-right-specific and 3 AFD-specific receptor-type guanylyl-cyclases. Late embryos exhibit a multipotential state in which AFD precursors transiently co-express all three types of ASEL, ASER and AFD markers. A forward genetic screen for defects in ASER asymmetry identified a Ppa-DIE-1 homolog, whereas targeted mutations revealed the maintenance of AFD neuronal identity requires another terminal-selector, Ppa-TTX-1, and CNG channels, Ppa-TAX-2/TAX-4. Mutations in the microRNA miR-8345 and pash-1 responsible for miRNA-processing convert ASEL to ASER fate while changes to other conserved regions in the 3' UTR of the cog-1 homolog reveal multiple sites that act as a toggle between left/right ASE versus AFD identities. Together, these results demonstrate that P. pacificus deploys a miRNA-mediated regulatory repertoire to generate three distinct neuronal fates through the Ppa-cog-1 3' UTR as a key regulatory nexus.
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.