ArticleDevelopmental cell2025
Asymmetric partitioning of persistent paternal mitochondria during cell divisions safeguards embryo development and mitochondrial inheritance.
Article in Developmental cell, 2025. 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.
- RoundMi: A quantitative method to analyze mitochondrial morphology in mitotic cells.FEBS open bio · 2026Article
- ALKB-1-dependent tRNA methylation is required for efficient paternal mitochondrial elimination.Nature communications · 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
2 authors.
Funding
Abstract
Most eukaryotes inherit only maternal mitochondria. The reasons for paternal mitochondrial elimination and the impacts of persistent paternal mitochondria on animals remain elusive. We show that undegraded paternal mitochondria in autophagy-deficient C. elegans embryos are gradually excluded from germ blastomeres through asymmetric partitioning during cell divisions. The embryonic cortical flow drives anterior-directed movements of paternal mitochondria and contributes to their asymmetric apportioning between two daughter blastomeres. By contrast, autophagosome-enclosed paternal mitochondria cluster around and segregate with centrosomes during mitosis and are rapidly degraded through lysosomes concentrated near centrosomes. Failure to exclude persistent paternal mitochondria from the germ blastomere at first cleavage causes their enrichment in the descendant endomesodermal (EMS) blastomere, leading to elevated reactive oxygen species levels, elongated EMS lineage durations, and increased embryonic lethality, which antioxidant treatments can suppress. Thus, regulated paternal mitochondrial distribution away from germ blastomeres is a fail-safe mechanism, protecting embryo development and maternal mitochondrial inheritance.
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.