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Germline MET-2-LIN-3-LET-23 signaling axis governs nanoplastic-induced transgenerational reproductive toxicity in Caenorhabditis elegans
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Scientists found that tiny plastic particles (nanoplastics), at levels comparable to real-world pollution, can damage the reproductive systems of worms—and this damage gets passed down to their offspring and grandoffspring, even though those descendants were never directly exposed. The researchers pinpointed the exact chain of molecular signals responsible, showing the plastic exposure triggers a self-destruct process in reproductive cells that carries forward across generations. While this study was done in worms, not humans, it's a warning sign: the ever-growing amount of nanoplastics in our food, water, and air could potentially affect fertility not just
Chronic exposure to low concentrations of polystyrene nanoparticles (PS-NPs) can induce reproductive toxicity across multiple generations, yet the underlying molecular mechanisms remain poorly defined. Our previous studies showed that the parental germline EGF ligand LIN-3 could transgenerationally regulate PS-NPs-induced reproductive toxicity by targeting intestinal LET-23-DAF-16 or neuronal LET-23-DBL-1/DAF-7 signaling in the offspring. However, the offspring germline signaling cascade mediated by parental LIN-3 remained unclear. Using Caenorhabditis elegans as a model, the present study demonstrates that a germline MET-2-initiated, LIN-3-EGF-MAPK-LIN-1-mediated transgenerational signaling cascade is crucial for regulating PS-NPs-induced reproductive toxicity. Exposure to 1-10 μg/L PS-NPs caused dose-dependent defects in reproductive output and gonadal development in subsequent generations. RNA interference of key EGF pathway components, including lin-3, let-23, let-60, lin-45, mpk-1, and lin-1, significantly alleviated PS-NPs-induced reproductive toxicity. Moreover, parental germline LIN-3, epigenetically regulated by the H3K9 histone methyltransferase MET-2, transgenerationally activated the offspring germline EGF receptor LET-23, thereby modulating reproductive outcomes. Downstream, LIN-1 transmitted signals from the LET-23-LET-60-LIN-45-MPK-1 cascade and regulated the pro-apoptotic factors HUS-1 and EGL-1, leading to germline apoptosis in response to PS-NPs exposure. In summary, low-dose PS-NPs induce transgenerational reproductive toxicity by promoting germline apoptosis through activation of the MET-2-LIN-3-LET-23-LET-60-LIN-45-MPK-1-LIN-1-HUS-1/EGL-1 signaling axis, providing mechanistic insight into the multigenerational reproductive risks posed by nanoplastics in the range of μg L.
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Researchers discovered that a single exposure to nanoplastics in mother roundworms caused reproductive decline that persisted across four subsequent unexposed generations. The study found that nanoplastics triggered DNA damage and cell death in reproductive cells, with these effects passed down through epigenetic changes rather than direct nanoplastic transfer to offspring. This finding suggests that nanoplastic exposure may have lasting consequences for fertility that extend well beyond the initially exposed generation.
Activation of FGF signal in germline mediates transgenerational toxicity of polystyrene nanoparticles at predicted environmental concentrations in Caenorhabditis elegans
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Using the roundworm C. elegans as a model, researchers investigated how nanoplastic exposure causes toxic effects that persist across generations. They found that polystyrene nanoparticles activate a specific growth factor signaling pathway in reproductive cells, which then transmits harmful effects to offspring. The study provides molecular evidence for how even low, environmentally relevant concentrations of nanoplastics can cause damage that carries over to future generations.
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Researchers found that nanoplastics at levels commonly found in the environment activated a specific genetic signaling pathway in roundworms that caused toxic effects passed down across multiple generations. The nanoplastics triggered changes in gene regulation that affected offspring who were never directly exposed to the plastic particles. This is particularly alarming because it suggests that nanoplastic exposure could have health consequences not just for the individual exposed but for their children and grandchildren through inherited genetic changes.
Parental Exposure to Nanoplastics and Graphene Oxide Induces Transgenerational Toxicity in Caenorhabditis elegans
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Scientists exposed tiny worms to nanoplastics and graphene oxide (materials found in plastic pollution and some industrial products) and found the damage—cell stress that harms growth, movement, and reproduction—was passed down to offspring who were never directly exposed. While this study was done in worms, not humans, it raises concerns that plastic pollution exposure could have effects that ripple into future generations, which is important as we consider the real-world health impact of ever-increasing plastic waste in our environment.
Amino-modified nanoplastics at predicted environmental concentrations cause transgenerational toxicity through activating germline EGF signal in Caenorhabditis elegans
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Researchers found that amino-modified nanoplastics, even at concentrations expected in the real environment, can cause toxic effects that pass from one generation to the next in the roundworm C. elegans. The transgenerational harm was linked to activation of a specific growth factor signal in reproductive cells. The study suggests that surface chemistry on nanoplastics may amplify their biological risks beyond what the base plastic alone would cause.
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