Acetochlor disrupts the maternal effect of food restriction in lizards (Eremias argus): Evidence from intergenerational growth and embryonic development.

Reptiles face an increasing risk of extinction, threatening global biodiversity. Although maternal effects are critical for intergenerational adaptation, whether environmental pollutants disrupt these mechanisms and compromise population adaptability remains unclear. This study examined whether acetochlor (ACE) disrupts maternal effects triggered by food restriction in lizards and assessed its consequences on offspring growth and development. The experiment exposed female lizards during the breeding season to ACE and food restriction, and their offspring (F1 generation) received no further treatment after hatching. Research findings indicate that when subjected to food restriction, mothers enhance offspring hatchability by increasing resource investment in eggs. However, ACE exposure disrupted this adaptive maternal strategy by altering key egg yolk metabolites and inhibiting the Wnt/β-catenin pathway, resulting in lower hatching rates and stunted offspring growth. This interference may be linked to ACE-induced endocrine disruption and oxidative stress in mothers. Further research found that acetochlor induces gut dysbiosis, reducing short-chain fatty acids and altering monoamine neurotransmitters, thereby impairing predatory capacity under food restriction. Meanwhile, gut pathogenic bacteria overgrowth reduces immunoglobulin Y levels in offspring. Acetochlor affected DNMT1 and DNMT3B, but food restriction affected DNMT3A. This study shows that ACE directly harms lizards and disrupts maternal adaptation to food restriction, threatening population resilience and providing a new mechanism for herbicide risk assessment.