ArticleCell communication and signaling : CCS2026
NANOS3-YTHDF2 drives aberrant P-body accumulation to impair folliculogenesis in offspring of maternal aristolochic acid I exposure.
Article in Cell communication and signaling : CCS, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Processing-bodies (PBs) are cytoplasmic membraneless condensates essential for RNA regulation. They share structural and functional similarities with germ granules and are critical for primordial folliculogenesis, a developmental process highly susceptible to exogenous insults. Aristolochic acid I (AAⅠ), a pervasive environmental toxin from Aristolochiaceae plants, is known to cross the placental barrier and induce fetal ovarian oxidative stress. Here, using a mouse model of maternal AAⅠ exposure (16.5 to 18.5 days post-coitus), we demonstrate that this prenatal insult causes profound defects in offspring folliculogenesis. AAⅠ induces PB enlargement and protein accumulation, causing these condensates to acquire germ granule-like properties. Specifically, AAⅠ upregulates the germ granule component NANOS3 to drive condensate enlargement. Multi-omic profiling further revealed that these aberrant condensates recruit germ granule-associated proteins and exhibit altered RNA profiles. Concurrently, neonatal oocytes exhibited enlarged Balbiani body-like structures alongside intermitochondrial cement, a feature not previously reported in oocytes. Furthermore, AAⅠ promotes the recruitment of N6-methyladenosine (m
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